Formation and development of a thrombus or blood clot in the blood vessel.
The formation or presence of a blood clot (THROMBUS) within a vein.
Coagulation of blood in any of the CORONARY VESSELS. The presence of a blood clot (THROMBUS) often leads to MYOCARDIAL INFARCTION.
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.
Formation or presence of a blood clot (THROMBUS) in a blood vessel within the SKULL. Intracranial thrombosis can lead to thrombotic occlusions and BRAIN INFARCTION. The majority of the thrombotic occlusions are associated with ATHEROSCLEROSIS.
Blood clot formation in any part of the CAROTID ARTERIES. This may produce CAROTID STENOSIS or occlusion of the vessel, leading to TRANSIENT ISCHEMIC ATTACK; CEREBRAL INFARCTION; or AMAUROSIS FUGAX.
Agents that prevent clotting.
Formation or presence of a blood clot (THROMBUS) in the SUPERIOR SAGITTAL SINUS or the inferior sagittal sinus. Sagittal sinus thrombosis can result from infections, hematological disorders, CRANIOCEREBRAL TRAUMA; and NEUROSURGICAL PROCEDURES. Clinical features are primarily related to the increased intracranial pressure causing HEADACHE; NAUSEA; and VOMITING. Severe cases can evolve to SEIZURES or COMA.
Radiographic visualization or recording of a vein after the injection of contrast medium.
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.
A vein on either side of the body which is formed by the union of the external and internal iliac veins and passes upward to join with its fellow of the opposite side to form the inferior vena cava.
A disorder of HEMOSTASIS in which there is a tendency for the occurrence of THROMBOSIS.
The vein accompanying the femoral artery in the same sheath; it is a continuation of the popliteal vein and becomes the external iliac vein.
DEEP VEIN THROMBOSIS of an upper extremity vein (e.g., AXILLARY VEIN; SUBCLAVIAN VEIN; and JUGULAR VEINS). It is associated with mechanical factors (Upper Extremity Deep Vein Thrombosis, Primary) secondary to other anatomic factors (Upper Extremity Deep Vein Thrombosis, Secondary). Symptoms may include sudden onset of pain, warmth, redness, blueness, and swelling in the arm.
A short thick vein formed by union of the superior mesenteric vein and the splenic vein.
Veins draining the cerebrum.
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.
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.
Fibrinolysin or agents that convert plasminogen to FIBRINOLYSIN.
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.
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.
Formation or presence of a blood clot (THROMBUS) in the CAVERNOUS SINUS of the brain. Infections of the paranasal sinuses and adjacent structures, CRANIOCEREBRAL TRAUMA, and THROMBOPHILIA are associated conditions. Clinical manifestations include dysfunction of cranial nerves III, IV, V, and VI, marked periorbital swelling, chemosis, fever, and visual loss. (From Adams et al., Principles of Neurology, 6th ed, p711)
The process of the interaction of BLOOD COAGULATION FACTORS that results in an insoluble FIBRIN clot.
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).
The venous trunk which receives blood from the lower extremities and from the pelvic and abdominal organs.
Obstruction of a blood vessel (embolism) by a blood clot (THROMBUS) in the blood stream.
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.
Formation or presence of a blood clot (THROMBUS) in the LATERAL SINUSES. This condition is often associated with ear infections (OTITIS MEDIA or MASTOIDITIS) without antibiotic treatment. In developed nations, lateral sinus thrombosis can result from CRANIOCEREBRAL TRAUMA; BRAIN NEOPLASMS; NEUROSURGICAL PROCEDURES; THROMBOPHILIA; and other conditions. Clinical features include HEADACHE; VERTIGO; and increased intracranial pressure.
Duration of blood flow after skin puncture. This test is used as a measure of capillary and platelet function.
Surgical removal of an obstructing clot or foreign material from a blood vessel at the point of its formation. Removal of a clot arising from a distant site is called EMBOLECTOMY.
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.
Devices that provide support for tubular structures that are being anastomosed or for body cavities during skin grafting.
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)
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 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.
Veins which return blood from the intestines; the inferior mesenteric vein empties into the splenic vein, the superior mesenteric vein joins the splenic vein to form the portal vein.
The continuation of the axillary vein which follows the subclavian artery and then joins the internal jugular vein to form the brachiocephalic vein.
Stents that are covered with materials that are embedded with chemicals that are gradually released into the surrounding milieu.
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 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 vein formed by the union of the anterior and posterior tibial veins; it courses through the popliteal space and becomes the femoral vein.
Veins in the neck which drain the brain, face, and neck into the brachiocephalic or subclavian veins.
Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation.
Obstruction of a vein or VEINS (embolism) by a blood clot (THROMBUS) in the blood stream.
Bleeding or escape of blood from a vessel.
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.
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.)
Large endothelium-lined venous channels situated between the two layers of DURA MATER, the endosteal and the meningeal layers. They are devoid of valves and are parts of the venous system of dura mater. Major cranial sinuses include a postero-superior group (such as superior sagittal, inferior sagittal, straight, transverse, and occipital) and an antero-inferior group (such as cavernous, petrosal, and basilar plexus).
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.
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.
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.
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.
Elements of limited time intervals, contributing to particular results or situations.
Use of infusions of FIBRINOLYTIC AGENTS to destroy or dissolve thrombi in blood vessels or bypass grafts.
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.
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.
Short thick veins which return blood from the kidneys to the vena cava.
Vein formed by the union (at the hilus of the spleen) of several small veins from the stomach, pancreas, spleen and mesentery.
Ultrasonography applying the Doppler effect combined with real-time imaging. The real-time image is created by rapid movement of the ultrasound beam. A powerful advantage of this technique is the ability to estimate the velocity of flow from the Doppler shift frequency.
A condition in which the hepatic venous outflow is obstructed anywhere from the small HEPATIC VEINS to the junction of the INFERIOR VENA CAVA and the RIGHT ATRIUM. Usually the blockage is extrahepatic and caused by blood clots (THROMBUS) or fibrous webs. Parenchymal FIBROSIS is uncommon.
An absence or reduced level of Antithrombin III leading to an increased risk for thrombosis.
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.
The natural enzymatic dissolution of FIBRIN.
The venous trunk of the upper limb; a continuation of the basilar and brachial veins running from the lower border of the teres major muscle to the outer border of the first rib where it becomes the subclavian vein.
Obstruction of the flow in the SPLANCHNIC CIRCULATION by ATHEROSCLEROSIS; EMBOLISM; THROMBOSIS; STENOSIS; TRAUMA; and compression or intrinsic pressure from adjacent tumors. Rare causes are drugs, intestinal parasites, and vascular immunoinflammatory diseases such as PERIARTERITIS NODOSA and THROMBOANGIITIS OBLITERANS. (From Juergens et al., Peripheral Vascular Diseases, 5th ed, pp295-6)
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.
A condition caused by one or more episodes of DEEP VEIN THROMBOSIS, usually the blood clots are lodged in the legs. Clinical features include EDEMA; PAIN; aching; heaviness; and MUSCLE CRAMP in the leg. When severe leg swelling leads to skin breakdown, it is called venous STASIS ULCER.
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)
Placement of an intravenous CATHETER in the subclavian, jugular, or other central vein.
Obstruction of flow in biological or prosthetic vascular grafts.
A protein derived from FIBRINOGEN in the presence of THROMBIN, which forms part of the blood clot.
Mechanical devices inserted in the inferior vena cava that prevent the migration of blood clots from deep venous thrombosis of the leg.
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.
A condition characterized by a chronically swollen limb, often a leg with stasis dermatitis and ulcerations. This syndrome can appear soon after phlebitis or years later. Postphlebitic syndrome is the result of damaged or incompetent venous valves in the limbs. Distended, tortuous VARICOSE VEINS are usually present. Leg pain may occur after long period of standing.
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.
Surgical shunt allowing direct passage of blood from an artery to a vein. (From Dorland, 28th ed)
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.
An effective inhibitor of platelet aggregation commonly used in the placement of STENTS in CORONARY ARTERIES.
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.
The return of a sign, symptom, or disease after a remission.
Tomography using x-ray transmission and a computer algorithm to reconstruct the image.
Laboratory tests for evaluating the individual's clotting mechanism.
Dilation of an occluded coronary artery (or arteries) by means of a balloon catheter to restore myocardial blood supply.
A macrolide compound obtained from Streptomyces hygroscopicus that acts by selectively blocking the transcriptional activation of cytokines thereby inhibiting cytokine production. It is bioactive only when bound to IMMUNOPHILINS. Sirolimus is a potent immunosuppressant and possesses both antifungal and antineoplastic properties.
Catheters designed to be left within an organ or passage for an extended period of time.
Recurrent narrowing or constriction of a coronary artery following surgical procedures performed to alleviate a prior obstruction.
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.
Tight coverings for the foot and leg that are worn to aid circulation in the legs, and prevent the formation of EDEMA and DEEP VEIN THROMBOSIS. PNEUMATIC COMPRESSION STOCKINGS serve a similar purpose especially for bedridden patients, and following surgery.
A clinical syndrome characterized by repeated spontaneous hemorrhages and a remarkable increase in the number of circulating platelets.
Insertion of a catheter into a peripheral artery, vein, or airway for diagnostic or therapeutic purposes.
Endogenous substances, usually proteins, that are involved in the blood coagulation process.
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)
The degree to which BLOOD VESSELS are not blocked or obstructed.
The vessels carrying blood away from the capillary beds.
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.
Disease having a short and relatively severe course.
A subnormal level of BLOOD PLATELETS.
The long large endothelium-lined venous channel on the top outer surface of the brain. It receives blood from a vein in the nasal cavity, runs backwards, and gradually increases in size as blood drains from veins of the brain and the DURA MATER. Near the lower back of the CRANIUM, the superior sagittal sinus deviates to one side (usually the right) and continues on as one of the TRANSVERSE SINUSES.
The plan and delineation of prostheses in general or a specific prosthesis.
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.
The number of new cases of a given disease during a given period in a specified population. It also is used for the rate at which new events occur in a defined population. It is differentiated from PREVALENCE, which refers to all cases, new or old, in the population at a given time.
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.
A proteolytic enzyme in the serine protease family found in many tissues which converts PLASMINOGEN to FIBRINOLYSIN. It has fibrin-binding activity and is immunologically different from UROKINASE-TYPE PLASMINOGEN ACTIVATOR. The primary sequence, composed of 527 amino acids, is identical in both the naturally occurring and synthetic proteases.
Pathological processes which result in the partial or complete obstruction of ARTERIES. They are characterized by greatly reduced or absence of blood flow through these vessels. They are also known as arterial insufficiency.
Recording changes in electrical impedance between electrodes placed on opposite sides of a part of the body, as a measure of volume changes in the path of the current. (Stedman, 25th ed)
Material used for wrapping or binding any part of the body.
Instruments that generate intermittent forces, uniformed or graduated, to facilitate the emptying of VEINS. These devices are used to reduce limb EDEMA and prevent venous THROMBOEMBOLISM, such as deep vein thrombosis in the legs.
Device constructed of either synthetic or biological material that is used for the repair of injured or diseased blood vessels.
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.
NECROSIS of the MYOCARDIUM caused by an obstruction of the blood supply to the heart (CORONARY CIRCULATION).
An enzyme formed from PROTHROMBIN that converts FIBRINOGEN to FIBRIN.
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
The process whereby PLATELETS adhere to something other than platelets, e.g., COLLAGEN; BASEMENT MEMBRANE; MICROFIBRILS; or other "foreign" surfaces.
Radiography of blood vessels after injection of a contrast medium.
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)
The number of PLATELETS per unit volume in a sample of venous BLOOD.
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)
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.
Rare chronic inflammatory disease involving the small blood vessels. It is of unknown etiology and characterized by mucocutaneous ulceration in the mouth and genital region and uveitis with hypopyon. The neuro-ocular form may cause blindness and death. SYNOVITIS; THROMBOPHLEBITIS; gastrointestinal ulcerations; RETINAL VASCULITIS; and OPTIC ATROPHY may occur as well.
A high-molecular-weight plasma protein, produced by endothelial cells and megakaryocytes, that is part of the factor VIII/von Willebrand factor complex. The von Willebrand factor has receptors for collagen, platelets, and ristocetin activity as well as the immunologically distinct antigenic determinants. It functions in adhesion of platelets to collagen and hemostatic plug formation. The prolonged bleeding time in VON WILLEBRAND DISEASES is due to the deficiency of this factor.
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.
Radiography of the vascular system of the heart muscle after injection of a contrast medium.
Ultrasonography applying the Doppler effect, with the superposition of flow information as colors on a gray scale in a real-time image. This type of ultrasonography is well-suited to identifying the location of high-velocity flow (such as in a stenosis) or of mapping the extent of flow in a certain region.
A myeloproliferative disorder of unknown etiology, characterized by abnormal proliferation of all hematopoietic bone marrow elements and an absolute increase in red cell mass and total blood volume, associated frequently with splenomegaly, leukocytosis, and thrombocythemia. Hematopoiesis is also reactive in extramedullary sites (liver and spleen). In time myelofibrosis occurs.
The condition of an anatomical structure's being constricted beyond normal dimensions.
A branch of the celiac artery that distributes to the stomach, pancreas, duodenum, liver, gallbladder, and greater omentum.
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.
Ultrasonography applying the Doppler effect, with frequency-shifted ultrasound reflections produced by moving targets (usually red blood cells) in the bloodstream along the ultrasound axis in direct proportion to the velocity of movement of the targets, to determine both direction and velocity of blood flow. (Stedman, 25th ed)
Disorders or diseases associated with PUERPERIUM, the six-to-eight-week period immediately after PARTURITION in humans.
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.
The region of the lower limb in animals, extending from the gluteal region to the FOOT, and including the BUTTOCKS; HIP; and LEG.
Inorganic or organic compounds containing trivalent iron.
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.
Agents capable of exerting a harmful effect on the body.
Use or insertion of a tubular device into a duct, blood vessel, hollow organ, or body cavity for injecting or withdrawing fluids for diagnostic or therapeutic purposes. It differs from INTUBATION in that the tube here is used to restore or maintain patency in obstructions.
The use of ultrasound to guide minimally invasive surgical procedures such as needle ASPIRATION BIOPSY; DRAINAGE; etc. Its widest application is intravascular ultrasound imaging but it is useful also in urology and intra-abdominal conditions.
Radiography of the vascular system of the brain after injection of a contrast medium.
Platelet membrane glycoprotein complex important for platelet adhesion and aggregation. It is an integrin complex containing INTEGRIN ALPHAIIB and INTEGRIN BETA3 which recognizes the arginine-glycine-aspartic acid (RGD) sequence present on several adhesive proteins. As such, it is a receptor for FIBRINOGEN; VON WILLEBRAND FACTOR; FIBRONECTIN; VITRONECTIN; and THROMBOSPONDINS. A deficiency of GPIIb-IIIa results in GLANZMANN THROMBASTHENIA.
Death resulting from the presence of a disease in an individual, as shown by a single case report or a limited number of patients. This should be differentiated from DEATH, the physiological cessation of life and from MORTALITY, an epidemiological or statistical concept.
Cell adhesion molecule and CD antigen that mediates the adhesion of neutrophils and monocytes to activated platelets and endothelial cells.
Compounds, usually hormonal, taken orally in order to block ovulation and prevent the occurrence of pregnancy. The hormones are generally estrogen or progesterone or both.
Pathological outpouching or sac-like dilatation in the wall of any blood vessel (ARTERIES or VEINS) or the heart (HEART ANEURYSM). It indicates a thin and weakened area in the wall which may later rupture. Aneurysms are classified by location, etiology, or other characteristics.
Increased numbers of platelets in the peripheral blood. (Dorland, 27th ed)
The main artery of the thigh, a continuation of the external iliac artery.
Operative procedures for the treatment of vascular disorders.
Hemorrhagic and thrombotic disorders that occur as a consequence of inherited abnormalities in blood coagulation.
Studies which start with the identification of persons with a disease of interest and a control (comparison, referent) group without the disease. The relationship of an attribute to the disease is examined by comparing diseased and non-diseased persons with regard to the frequency or levels of the attribute in each group.
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 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)
Homopolymer of tetrafluoroethylene. Nonflammable, tough, inert plastic tubing or sheeting; used to line vessels, insulate, protect or lubricate apparatus; also as filter, coating for surgical implants or as prosthetic material. Synonyms: Fluoroflex; Fluoroplast; Ftoroplast; Halon; Polyfene; PTFE; Tetron.
Pathological processes of CORONARY ARTERIES that may derive from a congenital abnormality, atherosclerotic, or non-atherosclerotic cause.
Extracellular vesicles generated by the shedding of CELL MEMBRANE blebs.
Biocompatible materials usually used in dental and bone implants that enhance biologic fixation, thereby increasing the bond strength between the coated material and bone, and minimize possible biological effects that may result from the implant itself.
A member of the serpin family of proteins. It inhibits both the tissue-type and urokinase-type plasminogen activators.
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.
Surgical insertion of BLOOD VESSEL PROSTHESES to repair injured or diseased blood vessels.
A repeat operation for the same condition in the same patient due to disease progression or recurrence, or as followup to failed previous surgery.
Formation of an infarct, which is NECROSIS in tissue due to local ISCHEMIA resulting from obstruction of BLOOD CIRCULATION, most commonly by a THROMBUS or EMBOLUS.
A proteolytic enzyme that converts PLASMINOGEN to FIBRINOLYSIN where the preferential cleavage is between ARGININE and VALINE. It was isolated originally from human URINE, but is found in most tissues of most VERTEBRATES.
Enlarged and tortuous VEINS.
Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.
The transference of a part of or an entire liver from one human or animal to another.
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.
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.
Large veins on either side of the root of the neck formed by the junction of the internal jugular and subclavian veins. They drain blood from the head, neck, and upper extremities, and unite to form the superior vena cava.
A subclass of purinergic P2Y receptors that have a preference for ADP binding and are coupled to GTP-BINDING PROTEIN ALPHA SUBUNIT, GI. The P2Y12 purinergic receptors are found in PLATELETS where they play an important role regulating PLATELET ACTIVATION.
A collective term for pathological conditions which are caused by the formation of a blood clot (THROMBUS) in a blood vessel, or by blocking of a blood vessel with an EMBOLUS, undissolved materials in the blood stream.
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.
The veins and arteries of the HEART.
Non-invasive method of vascular imaging and determination of internal anatomy without injection of contrast media or radiation exposure. The technique is used especially in CEREBRAL ANGIOGRAPHY as well as for studies of other vascular structures.
Either of the two principal arteries on both sides of the neck that supply blood to the head and neck; each divides into two branches, the internal carotid artery and the external carotid artery.
The visualization of deep structures of the body by recording the reflections or echoes of ultrasonic pulses directed into the tissues. Use of ultrasound for imaging or diagnostic purposes employs frequencies ranging from 1.6 to 10 megahertz.
Surgical venous shunt between the portal and systemic circulation to effect decompression of the portal circulation. It is performed primarily in the treatment of bleeding esophageal varices resulting from portal hypertension. Types of shunt include portacaval, splenorenal, mesocaval, splenocaval, left gastric-caval (coronary-caval), portarenal, umbilicorenal, and umbilicocaval.
A device that substitutes for a heart valve. It may be composed of biological material (BIOPROSTHESIS) and/or synthetic material.
The time required by whole blood to produce a visible clot.
Impaired venous blood flow or venous return (venous stasis), usually caused by inadequate venous valves. Venous insufficiency often occurs in the legs, and is associated with EDEMA and sometimes with VENOUS STASIS ULCERS at the ankle.
Agents that affect the rate or intensity of cardiac contraction, blood vessel diameter, or blood volume.
Surgical procedure involving either partial or entire removal of the spleen.
A family of percutaneous techniques that are used to manage CORONARY OCCLUSION, including standard balloon angioplasty (PERCUTANEOUS TRANSLUMINAL CORONARY ANGIOPLASTY), the placement of intracoronary STENTS, and atheroablative technologies (e.g., ATHERECTOMY; ENDARTERECTOMY; THROMBECTOMY; PERCUTANEOUS TRANSLUMINAL LASER ANGIOPLASTY). PTCA was the dominant form of PCI, before the widespread use of stenting.
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.
Laboratory examination used to monitor and evaluate platelet function in a patient's blood.
A heterogeneous group of proteolytic enzymes that convert PLASMINOGEN to FIBRINOLYSIN. They are concentrated in the lysosomes of most cells and in the vascular endothelium, particularly in the vessels of the microcirculation.
Electropositive chemical elements characterized by ductility, malleability, luster, and conductance of heat and electricity. They can replace the hydrogen of an acid and form bases with hydroxyl radicals. (Grant & Hackh's Chemical Dictionary, 5th ed)
Non-invasive method of demonstrating internal anatomy based on the principle that atomic nuclei in a strong magnetic field absorb pulses of radiofrequency energy and emit them as radiowaves which can be reconstructed into computerized images. The concept includes proton spin tomographic techniques.
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.
Therapy for the insufficient cleansing of the BLOOD by the kidneys based on dialysis and including hemodialysis, PERITONEAL DIALYSIS, and HEMODIAFILTRATION.
Use of a balloon catheter for dilation of an occluded artery. It is used in treatment of arterial occlusive diseases, including renal artery stenosis and arterial occlusions in the leg. For the specific technique of BALLOON DILATION in coronary arteries, ANGIOPLASTY, BALLOON, CORONARY is available.
Streptococcal fibrinolysin . An enzyme produced by hemolytic streptococci. It hydrolyzes amide linkages and serves as an activator of plasminogen. It is used in thrombolytic therapy and is used also in mixtures with streptodornase (STREPTODORNASE AND STREPTOKINASE). EC 3.4.-.
Abnormal increase of resistance to blood flow within the hepatic PORTAL SYSTEM, frequently seen in LIVER CIRRHOSIS and conditions with obstruction of the PORTAL VEIN.
The vessels carrying blood away from the heart.
The domestic dog, Canis familiaris, comprising about 400 breeds, of the carnivore family CANIDAE. They are worldwide in distribution and live in association with people. (Walker's Mammals of the World, 5th ed, p1065)
Malfunction of implantation shunts, valves, etc., and prosthesis loosening, migration, and breaking.
In screening and diagnostic tests, the probability that a person with a positive test is a true positive (i.e., has the disease), is referred to as the predictive value of a positive test; whereas, the predictive value of a negative test is the probability that the person with a negative test does not have the disease. Predictive value is related to the sensitivity and specificity of the test.
An absence or reduced level of blood coagulation factor XII. It normally occurs in the absence of patient or family history of hemorrhagic disorders and is marked by prolonged clotting time.
A cyclodecane isolated from the bark of the Pacific yew tree, TAXUS BREVIFOLIA. It stabilizes MICROTUBULES in their polymerized form leading to cell death.
The vein which drains the foot and leg.
Tear or break of an organ, vessel or other soft part of the body, occurring in the absence of external force.
A nonparametric method of compiling LIFE TABLES or survival tables. It combines calculated probabilities of survival and estimates to allow for observations occurring beyond a measurement threshold, which are assumed to occur randomly. Time intervals are defined as ending each time an event occurs and are therefore unequal. (From Last, A Dictionary of Epidemiology, 1995)
Use of HIRUDINS as an anticoagulant in the treatment of cardiological and hematological disorders.
Studies in which subsets of a defined population are identified. These groups may or may not be exposed to factors hypothesized to influence the probability of the occurrence of a particular disease or other outcome. Cohorts are defined populations which, as a whole, are followed in an attempt to determine distinguishing subgroup characteristics.
Narrowing or constriction of a coronary artery.

Systemic infection with Alaria americana (Trematoda). (1/5349)

Alaria americana is a trematode, the adult of which is found in mammalian carnivores. The first case of disseminated human infection by the mesocercarial stage of this worm occurred in a 24-year-old man. The infection possibly was acquired by the eating of inadequately cooked frogs, which are intermediate hosts of the worm. The diagnosis was made during life by lung biopsy and confirmed at autopsy. The mesocercariae were present in the stomach wall, lymph nodes, liver, myocardium, pancreas and surrounding adipose tissue, spleen, kidney, lungs, brain and spinal cord. There was no host reaction to the parasites. Granulomas were present in the stomach wall, lymph nodes and liver, but the worms were not identified in them. Hypersensitivity vasculitis and a bleeding diathesis due to disseminated intravascular coagulation and a circulating anticoagulant caused his death 8 days after the onset of his illness.  (+info)

Antiphospholipid, anti-beta 2-glycoprotein-I and anti-oxidized-low-density-lipoprotein antibodies in antiphospholipid syndrome. (2/5349)

Antiphospholipid antibodies (aPL), anti-beta 2-glycoprotein I (anti-beta 2-GPI) and anti-oxidized-low-density lipoprotein (LDL) antibodies are all implicated in the pathogenesis of antiphospholipid syndrome. To investigate whether different autoantibodies or combinations thereof produced distinct effects related to their antigenic specificities, we examined the frequencies of antiphospholipid syndrome (APS)-related features in the presence of different antibodies [aPL, beta 2-GPI, anti-oxidized low density lipoprotein (LDL)] in 125 patients with APS. Median follow-up was 72 months: 58 patients were diagnosed as primary APS and 67 as APS plus systemic lupus erythematosus (SLE). Anticardiolipin antibodies (aCL), anti-beta 2-GPI and anti-oxidized LDL antibodies were determined by ELISA; lupus anticoagulant (LA) by standard coagulometric methods. Univariate analysis showed that patients positive for anti-beta 2-GPI had a higher risk of recurrent thrombotic events (OR = 3.64, 95% CI, p = 0.01) and pregnancy loss (OR = 2.99, 95% CI, p = 0.004). Patients positive for anti-oxidized LDL antibodies had a 2.24-fold increase in the risk of arterial thrombosis (2.24, 95% CI, p = 0.03) and lower risk of thrombocytopenia (OR = 0.41 95% CI, p = 0.04). Patients positive for aCL antibodies had a higher risk of pregnancy loss (OR = 4.62 95% CI, p = 0.001). When these data were tested by multivariate logistic regression, the association between anti-beta 2-GPI and pregnancy loss and the negative association between anti-oxidized LDL antibodies and thrombocytopenia disappeared.  (+info)

Blood-borne tissue factor: another view of thrombosis. (3/5349)

Arterial thrombosis is considered to arise from the interaction of tissue factor (TF) in the vascular wall with platelets and coagulation factors in circulating blood. According to this paradigm, coagulation is initiated after a vessel is damaged and blood is exposed to vessel-wall TF. We have examined thrombus formation on pig arterial media (which contains no stainable TF) and on collagen-coated glass slides (which are devoid of TF) exposed to flowing native human blood. In both systems the thrombi that formed during a 5-min perfusion stained intensely for TF, much of which was not associated with cells. Antibodies against TF caused approximately 70% reduction in the amount of thrombus formed on the pig arterial media and also reduced thrombi on the collagen-coated glass slides. TF deposited on the slides was active, as there was abundant fibrin in the thrombi. Factor VIIai, a potent inhibitor of TF, essentially abolished fibrin production and markedly reduced the mass of the thrombi. Immunoelectron microscopy revealed TF-positive membrane vesicles that we frequently observed in large clusters near the surface of platelets. TF, measured by factor Xa formation, was extracted from whole blood and plasma of healthy subjects. By using immunostaining, TF-containing neutrophils and monocytes were identified in peripheral blood; our data raise the possibility that leukocytes are the main source of blood TF. We suggest that blood-borne TF is inherently thrombogenic and may be involved in thrombus propagation at the site of vascular injury.  (+info)

Endothelial implants inhibit intimal hyperplasia after porcine angioplasty. (4/5349)

The perivascular implantation of tissue-engineered endothelial cells around injured arteries offers an opportunity to study fundamental vascular physiology as well as restore and improve tissue function. Cell source is an important issue because the ability to implant either xenogeneic or allogeneic cells would greatly enhance the clinical applications of tissue-engineered grafts. We investigated the biological and immunological responses to endothelial cell xenografts and allografts in pigs 4 weeks after angioplasty of the carotid arteries. Porcine or bovine aortic endothelial cells were cultured within Gelfoam matrices and implanted in the perivascular space of 42 injured arteries. Both porcine and bovine endothelial cell grafts reduced the restenosis index compared with control by 54% and 46%, respectively. Perivascular heparin release devices, formulated to release heparin at twice the rate of release of heparan sulfate proteoglycan from endothelial cell implants, produced no significant reduction in the restenosis index. Endothelial cell implants also reduced occlusive thrombosis compared with control and heparin release devices. Host immune responses to endothelial implants were investigated by immunohistochemical examination of explanted devices and by immunocytochemistry of serum samples. The bovine cell grafts displayed infiltration of leukocytes, consisting primarily of lymphocytes, and caused an increase in antibodies detected in serum samples. Reduced cellular infiltration and no humoral response were detected in animals that received allografts. Despite the difference in immune response, the biological effects of xenografts or allografts did not differ significantly.  (+info)

The tourniquet in total knee arthroplasty. A prospective, randomised study. (5/5349)

We assessed the influence of the use of a tourniquet in total knee arthroplasty in a prospective, randomised study. After satisfying exclusion criteria, we divided 77 patients into two groups, one to undergo surgery with a tourniquet and one without. Both groups were well matched. The mean change in knee flexion in the group that had surgery without a tourniquet was significantly better at one week (p = 0.03) than in the other group, but movement was similar at six weeks and at four months. There was no significant difference in the surgical time, postoperative pain, need for analgesia, the volume collected in the drains, postoperative swelling, and the incidence of wound complications or of deep-venous thrombosis. We conclude that the use of a tourniquet is safe and that current practice can be continued.  (+info)

The value of late computed tomographic scanning in identification of vascular abnormalities after abdominal aortic aneurysm repair. (6/5349)

PURPOSE: The purpose of this study was to determine the prevalence of late arterial abnormalities after aortic aneurysm repair and thus to suggest a routine for postoperative radiologic follow-up examination and to establish reference criteria for endovascular repair. METHODS: Computed tomographic (CT) scan follow-up examination was obtained at 8 to 9 years after abdominal aortic aneurysm (AAA) repair on a cohort of patients enrolled in the Canadian Aneurysm Study. The original registry consisted of 680 patients who underwent repair of nonruptured AAA. When the request for CT scan follow-up examination was sent in 1994, 251 patients were alive and potentially available for CT scan follow-up examination and 94 patients agreed to undergo abdominal and thoracic CT scanning procedures. Each scan was interpreted independently by two vascular radiologists. RESULTS: For analysis, the aorta was divided into five defined segments and an aneurysm was defined as a more than 50% enlargement from the expected normal value as defined in the reporting standards for aneurysms. With this strict definition, 64.9% of patients had aneurysmal dilatation and the abnormality was considered as a possible indication for surgical repair in 13.8%. Of the 39 patients who underwent initial repair with a tube graft, 12 (30.8%) were found to have an iliac aneurysm and six of these aneurysms (15.4%) were of possible surgical significance. Graft dilatation was observed from the time of operation (median graft size of 18 mm) to a median size of 22 mm as measured by means of CT scanning at follow-up examination. Fluid or thrombus was seen around the graft in 28% of the cases, and bowel was believed to be intimately associated with the graft in 7%. CONCLUSION: Late follow-up CT scans after AAA repair often show vascular abnormalities. Most of these abnormalities are not clinically significant, but, in 13.8% of patients, the thoracic or abdominal aortic segment was aneurysmal and, in 15.4% of patients who underwent tube graft placement, one of the iliac arteries was significantly abnormal to warrant consideration for surgical repair. On the basis of these findings, a routine CT follow-up examination after 5 years is recommended. This study provides a population-based study for comparison with the results of endovascular repair.  (+info)

Immunohistochemical analysis of arterial wall cellular infiltration in Buerger's disease (endarteritis obliterans). (7/5349)

PURPOSE: The diagnosis of Buerger's disease has depended on clinical symptoms and angiographic findings, whereas pathologic findings are considered to be of secondary importance. Arteries from patients with Buerger's tissue were analyzed histologically, including immunophenotyping of the infiltrating cells, to elucidate the nature of Buerger's disease as a vasculitis. METHODS: Thirty-three specimens from nine patients, in whom Buerger's disease was diagnosed on the basis of our clinical and angiographic criteria between 1980 and 1995 at Nagoya University Hospital, were studied. Immunohistochemical studies were performed on paraffin-embedded tissue with a labeled streptoavidin-biotin method. RESULTS: The general architecture of vessel walls was well preserved regardless of the stage of disease, and cell infiltration was observed mainly in the thrombus and the intima. Among infiltrating cells, CD3(+) T cells greatly outnumbered CD20(+) B cells. CD68(+) macrophages or S-100(+) dendritic cells were detected, especially in the intima during acute and subacute stages. All cases except one showed infiltration by the human leukocyte antigen-D region (HLA-DR) antigen-bearing macrophages and dendritic cells in the intima. Immunoglobulins G, A, and M (IgG, IgA, IgM) and complement factors 3d and 4c (C3d, C4c) were deposited along the internal elastic lamina. CONCLUSION: Buerger's disease is strictly an endarteritis that is introduced by T-cell mediated cellular immunity and by B-cell mediated humoral immunity associated with activation of macrophages or dendritic cells in the intima.  (+info)

The intrarenal vascular lesions associated with primary antiphospholipid syndrome. (8/5349)

Even 10 yr after the identification of the antiphospholipid syndrome (APS), renal involvement in the course of APS is still relatively unrecognized, and is probably underestimated. The association of anticardiolipin antibodies and/or lupus anticoagulant with the development of a vaso-occlusive process involving numerous organs is now confirmed. In a multicenter study, 16 cases of "primary" APS (PAPS) were found and followed for 5 yr or more, all with renal biopsy. In all 16 cases of PAPS, there was a vascular nephropathy characterized by small vessel vaso-occlusive lesions associated with fibrous intimal hyperplasia of interlobular arteries (12 patients), recanalizing thrombi in arteries and arterioles (six patients), and focal cortical atrophy (10 patients). In combination, these led to progressive destruction of the kidney, accelerated by acute glomerular and arteriolar microangiopathy in five patients. Focal cortical atrophy is a distinctive lesion, present in 10 biopsies, and likely represents the histologic and functional renal analogue to the multiple cerebral infarcts detected on imaging studies. The clinical hallmark of this vascular nephropathy in PAPS is systemic hypertension, only variably associated with renal insufficiency, proteinuria, or hematuria. The ensemble of histologic renal lesions defined in this study should aid in the separation of the lesions found in cases of secondary APS, especially systemic lupus erythematosus, into those lesions related to APS and those related to the underlying disease.  (+info)

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.

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.

Coronary Thrombosis can cause a range of symptoms including chest pain, shortness of breath, lightheadedness and fatigue. The severity of the symptoms depends on the location and size of the clot. In some cases, the condition may be asymptomatic and diagnosed incidentally during a medical examination or imaging test.

Diagnosis of Coronary Thrombosis is typically made using electrocardiogram (ECG), blood tests and imaging studies such as angiography or echocardiography. Treatment options include medications to dissolve the clot, surgery to open or bypass the blocked artery or other interventional procedures such as angioplasty or stenting.

Prevention of Coronary Thrombosis includes managing risk factors such as high blood pressure, high cholesterol levels, smoking and diabetes through lifestyle changes and medications. Early detection and treatment can help reduce the risk of complications and improve outcomes for patients with this condition.

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 thrombosis, including:

1. Cerebral venous sinus thrombosis (CVST): This type of thrombosis occurs when a blood clot forms in the veins that drain blood from the brain. CVST is more common in young adults and is often associated with certain risk factors, such as cancer, infection, or trauma.
2. Cerebral arterial thrombosis (CAT): This type of thrombosis occurs when a blood clot forms in an artery that supplies blood to the brain. CAT is more common in older adults and is often associated with risk factors such as high blood pressure, diabetes, or heart disease.
3. Pial sinus thrombosis: This type of thrombosis occurs when a blood clot forms in the pial sinuses, which are specialized blood vessels that surround the brain. Pial sinus thrombosis is more common in children and young adults.

The symptoms of intracranial thrombosis can vary depending on the location and size of the clot, but may include:

1. Headache: A severe headache is often the first symptom of intracranial thrombosis. The headache may be sudden and severe, or it may develop gradually over time.
2. Confusion: Patients with intracranial thrombosis may experience confusion, disorientation, or difficulty concentrating.
3. Weakness or numbness: Patients may experience weakness or numbness in their arms, legs, or face on one side of the body.
4. Vision problems: Intracranial thrombosis can cause vision problems, such as blurred vision, double vision, or loss of peripheral vision.
5. Speech difficulties: Patients may experience difficulty speaking or understanding speech.
6. Seizures: In some cases, intracranial thrombosis can cause seizures.
7. Fever: Patients with intracranial thrombosis may develop a fever, especially if the clot is infected.
8. Weakness in the limbs: Patients may experience weakness or paralysis in their arms or legs.
9. Difficulty swallowing: Patients may have difficulty swallowing or experience drooling.
10. Change in mental status: Patients with intracranial thrombosis may exhibit changes in their mental status, such as lethargy, agitation, or confusion.

If you or someone you know is experiencing these symptoms, it is important to seek medical attention immediately. Intracranial thrombosis can be diagnosed through imaging tests such as CT or MRI scans, and treated with anticoagulant medications, thrombolysis, or surgery. Early diagnosis and treatment can help prevent long-term damage and improve outcomes for patients.

Carotid artery thrombosis is often caused by atherosclerosis, which is the buildup of plaque in the arteries that can lead to the formation of blood clots. Other risk factors for carotid artery thrombosis include high blood pressure, smoking, high cholesterol, diabetes, and obesity.

Diagnosis of carotid artery thrombosis typically involves imaging tests such as ultrasound, CT or MRI scans, and Doppler studies to visualize the blood flow in the neck and brain. Treatment options for carotid artery thrombosis include anticoagulation medications to prevent further clotting, medications to dissolve the clot, and surgery to remove the clot or repair the affected artery.

In severe cases, carotid artery thrombosis can lead to stroke or brain damage if not treated promptly. Therefore, it is important to seek medical attention immediately if symptoms persist or worsen over time.

Causes:

The exact cause of SST is not well understood, but it is believed to be related to abnormal blood flow or coagulation disorders. Some possible causes include:

* Infection: Bacterial, viral, or fungal infections can cause inflammation and damage to the blood vessels in the brain, leading to the formation of a clot in the sagittal sinus.
* Trauma: Head injuries or other types of trauma can cause damage to the blood vessels in the brain, leading to the formation of a clot in the sagittal sinus.
* Genetic predisposition: Some people may be born with a genetic predisposition to develop SST.
* Cancer: Certain types of cancer, such as lymphoma or leukemia, can cause abnormal blood flow and increase the risk of SST.

Symptoms:

The symptoms of SST can vary depending on the location and size of the clot. Some common symptoms include:

* Headache: A severe headache is often the first symptom of SST, which may be accompanied by nausea and vomiting.
* Seizures: SST can cause seizures, especially in children.
* Confusion: Patients with SST may experience confusion, disorientation, and difficulty concentrating.
* Weakness or paralysis: Depending on the location of the clot, patients may experience weakness or paralysis in the arms, legs, or face.
* Vision problems: SST can cause vision problems, including blurred vision, double vision, or loss of peripheral vision.

Diagnosis:

SST is difficult to diagnose, as the symptoms can be similar to other conditions such as meningitis or stroke. A thorough physical examination and imaging studies are necessary to confirm the diagnosis. Some common diagnostic tests include:

* Computed tomography (CT) scan: A CT scan can help identify the location and size of the clot.
* Magnetic resonance imaging (MRI): An MRI can provide more detailed information about the clot and its effects on surrounding tissue.
* Doppler ultrasound: A Doppler ultrasound can help identify blood flow in the affected area.

Treatment:

The treatment of SST depends on the location and size of the clot, as well as the underlying cause. Some common treatment options include:

* Anticoagulant medications: These medications, such as heparin or warfarin, can help prevent further clotting.
* Thrombolytic medications: These medications, such as tissue plasminogen activator (tPA), can dissolve the clot.
* Surgery: In some cases, surgery may be necessary to remove the clot or repair damaged blood vessels.

Complications:

SST can have serious complications, including:

* Stroke: If the clot blocks the flow of blood to the brain, it can cause a stroke.
* Heart attack: If the clot blocks the flow of blood to the heart, it can cause a heart attack.
* Pulmonary embolism: If the clot breaks loose and travels to the lungs, it can cause a pulmonary embolism.

Prevention:

To prevent SST, it is important to take steps to reduce your risk factors. This can include:

* Controlling high blood pressure
* Controlling high cholesterol levels
* Quitting smoking
* Maintaining a healthy weight
* Exercising regularly
* Avoiding long periods of immobility, such as during long-distance travel.

Prognosis:

The prognosis for SST is generally good if the clot is detected and treated early. However, if the clot is left untreated, it can lead to serious complications and can be fatal.

Lifestyle changes:

To reduce the risk of developing SST, you can make lifestyle changes such as:

* Quitting smoking
* Maintaining a healthy weight
* Exercising regularly
* Avoiding long periods of immobility, such as during long-distance travel.

Medications:

There are several medications that can be used to treat SST, including:

* Anticoagulants, such as warfarin or heparin, which prevent the clot from growing larger and prevent new clots from forming.
* Thrombolytics, such as tissue plasminogen activator (tPA), which dissolve the clot.
* Antiplatelet agents, such as aspirin, which prevent platelets from sticking together and forming a clot.

Surgery:

In some cases, surgery may be necessary to treat SST. This can include:

* Endovascular therapy, such as angioplasty or stenting, which can be used to open up the blocked blood vessel.
* Bypass surgery, which can be used to reroute blood flow around the blocked blood vessel.

Complications:

SST can cause a number of complications, including:

* Pulmonary embolism: If a piece of the clot breaks loose and travels to the lungs, it can cause a pulmonary embolism, which can be life-threatening.
* Stroke or brain damage: If the clot blocks blood flow to the brain, it can cause a stroke or brain damage.
* Infection: The clot can become infected, which can lead to sepsis and other complications.
* Amputation: In severe cases, SST can lead to tissue death and amputation of the affected limb.

Prognosis:

The prognosis for SST is generally good if the condition is diagnosed and treated promptly. However, if left untreated, it can lead to serious complications and even death. The overall survival rate for SST is about 80%.

Lifestyle Changes:

There are several lifestyle changes that can help reduce the risk of developing SST, including:

* Maintaining a healthy weight
* Exercising regularly
* Avoiding long periods of immobility, such as during long-distance travel.

Medications:

There are several medications that can be used to treat SST, including:

* Anticoagulants, which prevent the clot from growing and prevent new clots from forming.
* Thrombolytics, which dissolve the clot.
* Antiplatelet agents, which prevent platelets from sticking together and forming a clot.

Surgery:

In some cases, surgery may be necessary to treat SST. This can include:

* Thrombectomy, which involves removing the clot.
* Embolectomy, which involves removing the clot from the blood vessel.

Conclusion:

SST is a serious condition that can lead to severe complications if left untreated. However, with prompt diagnosis and treatment, the prognosis is generally good. Lifestyle changes and medications can help reduce the risk of developing SST, and surgery may be necessary in some cases. It is important to seek medical attention immediately if you experience any symptoms of SST.

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.

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.

Symptoms of UEDVT may include pain, swelling, redness, and warmth in the affected arm or shoulder. Diagnosis is typically made through imaging tests such as ultrasound or venography. Treatment may involve anticoagulation therapy to prevent the clot from growing and potentially breaking loose and traveling to the lungs. In some cases, a filter may be placed in the vena cava to prevent the clot from reaching the lungs.

Sources:

* Merriam-Webster's Medical Dictionary
* American College of Cardiology
* National Blood Clot Alliance

The cavernous sinus is a complex network of veins located in the brain that drain blood from the brain into the jugular vein. When a blood clot forms within the cavernous sinus, it can obstruct the flow of blood and cause a variety of complications.

There are several factors that can contribute to the development of CST, including:

1. Infection: Bacterial or viral infections can spread to the cavernous sinus and cause inflammation and clotting.
2. Trauma: Head trauma or injury can cause bleeding within the cavernous sinus.
3. Cancer: Certain types of cancer, such as brain tumors, can obstruct the flow of blood within the cavernous sinus.
4. Inherited disorders: Some inherited disorders, such as protein C or S deficiency, can increase the risk of developing CST.

Symptoms of CST can vary depending on the size and location of the clot, but may include:

1. Headache: A severe headache is a common symptom of CST, which can be worse with movement or exertion.
2. Seizures: CST can cause seizures, especially in children.
3. Vision loss: If the clot is located near the optic nerve, it can cause vision loss or blindness.
4. Fever: A fever can be a symptom of CST, especially if it is caused by an infection.
5. Weakness or numbness: Patients may experience weakness or numbness on one side of the body due to pressure on the brain.

Diagnosis of CST typically involves a combination of imaging studies, such as CT or MRI scans, and laboratory tests to rule out other conditions. Treatment options for CST include anticoagulation therapy, which can help dissolve the clot and prevent further blood clots from forming, and surgery to remove the clot. In some cases, patients may require supportive care, such as mechanical ventilation or dialysis, if other organs are affected by the clot.

Prevention of CST includes avoiding risk factors such as smoking, taking birth control pills, or having a history of blood clots in the family. Proper management of underlying medical conditions, such as atrial fibrillation or protein C or S deficiency, can also help prevent CST.

Prognosis for patients with CST depends on several factors, including the size and location of the clot, the age of the patient, and the presence of any underlying medical conditions. In general, early diagnosis and treatment improve the chances of a good outcome. However, CST can be a life-threatening condition if not properly treated, and patients may experience long-term effects such as cognitive impairment or seizures.

In summary, cerebral sinovenous thrombosis (CST) is a type of blood clot that forms in the venous sinuses of the brain, which can cause a variety of symptoms and complications. Diagnosis is typically made through imaging tests such as CT or MRI scans, and treatment may involve anticoagulant medications to dissolve the clot, surgery to remove the clot, or supportive care for affected organs. Prevention includes avoiding risk factors and properly managing underlying medical conditions, and prognosis depends on several factors including the size and location of the clot, the age of the patient, and the presence of any underlying medical conditions.

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.

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.

LST can be caused by a variety of factors, including head trauma, infection, inflammation, or cancer. It can also be associated with other conditions such as stroke, sepsis, or cancer.

Symptoms of LST can include headache, facial pain, swelling, and redness on the side of the head, and changes in mental status. In severe cases, LST can lead to brain abscess, meningitis, or stroke.

Diagnosis of LST is based on a combination of clinical examination, imaging studies such as CT or MRI scans, and laboratory tests. Treatment typically involves antibiotics for any underlying infection, and medications to dissolve blood clots. In severe cases, surgery may be necessary to remove the blood clot or repair any damage to the vein.

Prognosis for LST varies depending on the severity of the condition and the promptness and effectiveness of treatment. In general, early diagnosis and treatment improve the chances of a good outcome. However, LST can be a life-threatening condition, and mortality rates have been reported to range from 10% to 50%.

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.

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.

Example sentence: The patient had a hemorrhage after the car accident and needed immediate medical attention.

Word origin: [Latin] proteinus, "protein" + C, "deficiency"

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.

The condition is named after the German physician Hans von Budde and the Italian physician Giorgio Chiari, who independently described it in the late 19th century. It is also known as Budd-Chiari syndrome or venous sinus thrombosis.

The exact cause of Budd-Chiari Syndrome is not known, but it is thought to be related to a combination of genetic and environmental factors. Some cases have been linked to autoimmune disorders, such as lupus, or to infections, such as endocarditis.

Symptoms of Budd-Chiari Syndrome can vary in severity and may include:

* Headaches
* Facial swelling
* Difficulty swallowing
* Numbness or tingling in the face or limbs
* Vision problems
* Fatigue
* Shortness of breath

If you suspect that you or someone else may have Budd-Chiari Syndrome, it is important to seek medical attention as soon as possible. A healthcare provider can perform a physical examination and order diagnostic tests, such as imaging studies or blood tests, to confirm the diagnosis and determine the underlying cause.

Treatment for Budd-Chiari Syndrome typically involves addressing the underlying cause of the condition, such as antibiotics for an infection or medication to treat an autoimmune disorder. In some cases, a procedure called thrombectomy may be necessary to remove a blood clot that is blocking the veins.

In severe cases, Budd-Chiari Syndrome can lead to complications such as stroke or heart failure, so it is important to seek medical attention promptly if symptoms persist or worsen over time. With timely and appropriate treatment, however, many people with this condition are able to recover and manage their symptoms effectively.

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.

Mesenteric vascular occlusion can be caused by various factors, such as atherosclerosis (hardening of the arteries), blood clots, or inflammation. This condition can lead to a reduction in blood flow to the intestines, which can cause symptoms such as abdominal pain, diarrhea, and vomiting. In severe cases, it can also lead to tissue death and potentially life-threatening complications.

There are several types of mesenteric vascular occlusion, including:

1. Acute mesenteric ischemia (AMI): This is a sudden and severe blockage of the blood vessels that supply the intestines, which can cause tissue death and potentially life-threatening complications.
2. Chronic mesenteric ischemia (CMI): This is a gradual and less severe blockage of the blood vessels that supply the intestines, which can cause symptoms such as abdominal pain and diarrhea.
3. Mesenteric venous thrombosis: This is the formation of a blood clot in the veins that drain blood from the intestines.

Diagnosis of mesenteric vascular occlusion typically involves imaging tests such as CT or MRI scans, and blood tests to check for signs of inflammation or tissue damage. Treatment options vary depending on the severity and cause of the condition, and may include medications to dissolve blood clots, surgery to repair or bypass blocked blood vessels, or in severe cases, removal of the affected intestine.

The exact cause of PTS is not fully understood, but it is thought to be related to inflammation, damage to the vein wall, and abnormalities in blood flow. Risk factors for developing PTS include previous DVT, long-term immobility, obesity, and smoking.

Symptoms of PTS can vary in severity and may include:

* Pain or tenderness in the affected limb
* Swelling in the affected limb
* Skin discoloration (redness or bluing) in the affected limb
* Limited mobility or stiffness in the affected limb
* Cramping or aching pain in the affected limb
* Fatigue or weakness in the affected limb

PTS can be diagnosed through a physical examination, medical history, and imaging tests such as ultrasound or venography. Treatment for PTS typically involves anticoagulation therapy to prevent further clotting, compression stockings to reduce swelling, and pain management with medication or other interventions. In severe cases, surgery may be necessary to remove the clot or repair damaged veins.

Prevention of PTS is key, and this includes early diagnosis and treatment of DVT, avoiding long-term immobility, maintaining a healthy weight, and avoiding smoking. Managing underlying conditions such as cancer, autoimmune disorders, or inflammatory diseases can also help reduce the risk of developing PTS.

Overall, Postthrombotic Syndrome is a common complication of DVT that can have a significant impact on quality of life. Prompt diagnosis and appropriate treatment are essential to manage symptoms and prevent long-term morbidity.

Graft occlusion can occur due to a variety of factors, including:

1. Blood clots forming within the graft
2. Inflammation or infection within the graft
3. Narrowing or stenosis of the graft
4. Disruption of the graft material
5. Poor blood flow through the graft

The signs and symptoms of vascular graft occlusion can vary depending on the location and severity of the blockage. They may include:

1. Pain or tenderness in the affected limb
2. Swelling or redness in the affected limb
3. Weakness or numbness in the affected limb
4. Difficulty walking or moving the affected limb
5. Coolness or discoloration of the skin in the affected limb

If you experience any of these symptoms, it is important to seek medical attention as soon as possible. A healthcare professional can diagnose vascular graft occlusion using imaging tests such as ultrasound, angiography, or MRI. Treatment options for vascular graft occlusion may include:

1. Medications to dissolve blood clots or reduce inflammation
2. Surgical intervention to repair or replace the graft
3. Balloon angioplasty or stenting to open up the blocked graft
4. Hyperbaric oxygen therapy to improve blood flow and promote healing.

Preventive measures to reduce the risk of vascular graft occlusion include:

1. Proper wound care and infection prevention after surgery
2. Regular follow-up appointments with your healthcare provider
3. Avoiding smoking and other cardiovascular risk factors
4. Taking medications as directed by your healthcare provider to prevent blood clots and inflammation.

It is important to note that vascular graft occlusion can be a serious complication after surgery, but with prompt medical attention and appropriate treatment, the outcome can be improved.

The exact cause of postphlebitic syndrome is not known, but it is thought to be due to inflammation and scarring in the vein wall after a DVT has resolved. The condition can develop months or even years after the initial DVT and can affect one or both legs.

Symptoms of postphlebitic syndrome may include:

1. Chronic pain or tenderness in the affected limb
2. Swelling, redness, and warmth in the affected limb
3. Skin discoloration (hypo-pigmentation) or hyper-pigmentation in the affected limb
4. Limited mobility or stiffness in the affected limb
5. Fatigue
6. Night cramps
7. Muscle weakness
8. Raynaud's phenomenon (abnormal blood flow to the fingers and toes)

Postphlebitic syndrome can be difficult to diagnose, as the symptoms can be similar to other conditions such as chronic venous insufficiency or peripheral artery disease. A healthcare provider will typically perform a physical examination and order imaging tests such as ultrasound or venography to confirm the diagnosis.

Treatment for postphlebitic syndrome is focused on relieving symptoms and improving quality of life. This may include:

1. Pain management with medication or compression stockings
2. Elevating the affected limb to reduce swelling
3. Compression stockings to improve blood flow
4. Physical therapy to improve mobility and strength
5. Wound care if there are any open sores
6. Anticoagulation therapy to prevent future DVTs

Early diagnosis and treatment of postphlebitic syndrome can help improve symptoms and quality of life for individuals affected by the condition.

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.

Coronary restenosis is a common complication after coronary interventions, such as angioplasty or stenting. It is estimated that up to 20% of patients may experience restenosis within six months after treatment. If left untreated, restenosis can lead to chest pain, heart attack, or even death.

Treatment options for coronary restenosis include repeat angioplasty or stenting, medications such as beta blockers and calcium channel blockers, or bypass surgery. It is important for patients to work closely with their healthcare provider to monitor their symptoms and undergo regular follow-up appointments to prevent or diagnose restenosis early on.

1. Primary essential thrombocythemia (PET): This is the more common form, usually occurring spontaneously without any identifiable cause. Symptoms may include headache, migraine, seizures, and stroke-like episodes.
2. Secondary essential thrombocythemia: This form is caused by another medical condition or medication that stimulates the production of platelets. Symptoms are similar to those of PET, but there may be an underlying cause such as a tumor or an adverse reaction to medication.

Treatment for essential thrombocythemia includes medications to reduce platelet count and prevent blood clots, as well as close monitoring and management of any underlying causes. In some cases, surgery may be necessary to remove a tumor or other contributing factor.

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.

Examples of acute diseases include:

1. Common cold and flu
2. Pneumonia and bronchitis
3. Appendicitis and other abdominal emergencies
4. Heart attacks and strokes
5. Asthma attacks and allergic reactions
6. Skin infections and cellulitis
7. Urinary tract infections
8. Sinusitis and meningitis
9. Gastroenteritis and food poisoning
10. Sprains, strains, and fractures.

Acute diseases can be treated effectively with antibiotics, medications, or other therapies. However, if left untreated, they can lead to chronic conditions or complications that may require long-term care. Therefore, it is important to seek medical attention promptly if symptoms persist or worsen over time.

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.

Types of Arterial Occlusive Diseases:

1. Atherosclerosis: Atherosclerosis is a condition where plaque builds up inside the arteries, leading to narrowing or blockages that can restrict blood flow to certain areas of the body.
2. Peripheral Artery Disease (PAD): PAD is a condition where the blood vessels in the legs and arms become narrowed or blocked, leading to pain or cramping in the affected limbs.
3. Coronary Artery Disease (CAD): CAD is a condition where the coronary arteries, which supply blood to the heart, become narrowed or blocked, leading to chest pain or a heart attack.
4. Carotid Artery Disease: Carotid artery disease is a condition where the carotid arteries, which supply blood to the brain, become narrowed or blocked, leading to stroke or mini-stroke.
5. Renal Artery Stenosis: Renal artery stenosis is a condition where the blood vessels that supply the kidneys become narrowed or blocked, leading to high blood pressure and decreased kidney function.

Symptoms of Arterial Occlusive Diseases:

1. Pain or cramping in the affected limbs
2. Weakness or fatigue
3. Difficulty walking or standing
4. Chest pain or discomfort
5. Shortness of breath
6. Dizziness or lightheadedness
7. Stroke or mini-stroke

Treatment for Arterial Occlusive Diseases:

1. Medications: Medications such as blood thinners, cholesterol-lowering drugs, and blood pressure medications may be prescribed to treat arterial occlusive diseases.
2. Lifestyle Changes: Lifestyle changes such as quitting smoking, exercising regularly, and eating a healthy diet can help manage symptoms and slow the progression of the disease.
3. Endovascular Procedures: Endovascular procedures such as angioplasty and stenting may be performed to open up narrowed or blocked blood vessels.
4. Surgery: In some cases, surgery may be necessary to treat arterial occlusive diseases, such as bypass surgery or carotid endarterectomy.

Prevention of Arterial Occlusive Diseases:

1. Maintain a healthy diet and lifestyle
2. Quit smoking and avoid exposure to secondhand smoke
3. Exercise regularly
4. Manage high blood pressure, high cholesterol, and diabetes
5. Avoid excessive alcohol consumption
6. Get regular check-ups with your healthcare provider

Early detection and treatment of arterial occlusive diseases can help manage symptoms, slow the progression of the disease, and prevent complications such as heart attack or stroke.

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.

There are different types of myocardial infarctions, including:

1. ST-segment elevation myocardial infarction (STEMI): This is the most severe type of heart attack, where a large area of the heart muscle is damaged. It is characterized by a specific pattern on an electrocardiogram (ECG) called the ST segment.
2. Non-ST-segment elevation myocardial infarction (NSTEMI): This type of heart attack is less severe than STEMI, and the damage to the heart muscle may not be as extensive. It is characterized by a smaller area of damage or a different pattern on an ECG.
3. Incomplete myocardial infarction: This type of heart attack is when there is some damage to the heart muscle but not a complete blockage of blood flow.
4. Collateral circulation myocardial infarction: This type of heart attack occurs when there are existing collateral vessels that bypass the blocked coronary artery, which reduces the amount of damage to the heart muscle.

Symptoms of a myocardial infarction can include chest pain or discomfort, shortness of breath, lightheadedness, and fatigue. These symptoms may be accompanied by anxiety, fear, and a sense of impending doom. In some cases, there may be no noticeable symptoms at all.

Diagnosis of myocardial infarction is typically made based on a combination of physical examination findings, medical history, and diagnostic tests such as an electrocardiogram (ECG), cardiac enzyme tests, and imaging studies like echocardiography or cardiac magnetic resonance imaging.

Treatment of myocardial infarction usually involves medications to relieve pain, reduce the amount of work the heart has to do, and prevent further damage to the heart muscle. These may include aspirin, beta blockers, ACE inhibitors or angiotensin receptor blockers, and statins. In some cases, a procedure such as angioplasty or coronary artery bypass surgery may be necessary to restore blood flow to the affected area.

Prevention of myocardial infarction involves managing risk factors such as high blood pressure, high cholesterol, smoking, diabetes, and obesity. This can include lifestyle changes such as a healthy diet, regular exercise, and stress reduction, as well as medications to control these conditions. Early detection and treatment of heart disease can help prevent myocardial infarction from occurring in the first place.

1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.

2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.

3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.

4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.

5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.

6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.

7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.

8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.

9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.

10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.

Note: This definition is based on the current medical knowledge and may change as new research and discoveries are made.

The symptoms of Behcet syndrome can vary widely, but may include:

* Skin lesions, such as ulcers or rashes
* Eye inflammation (uveitis)
* Joint pain and swelling
* Digestive problems such as diarrhea and abdominal pain
* Nervous system problems such as seizures and headaches
* Inflammation of the blood vessels, which can lead to aneurysms or blood clots

The exact cause of Behcet syndrome is not known, but it is believed to be related to a combination of genetic and environmental factors. There is no cure for the disease, but various treatments are available to manage the symptoms and prevent complications. These may include medications such as corticosteroids, immunosuppressive drugs, and antibiotics, as well as lifestyle modifications such as avoiding triggers like spicy foods or stress.

Behcet syndrome is rare in the United States, but it is more common in certain parts of the world, including Turkey, Japan, and other countries with high prevalence of autoimmune disorders. It affects both men and women equally, and typically begins during adulthood, although it can sometimes begin in childhood or adolescence.

Overall, Behcet syndrome is a complex and multifaceted disease that requires careful management by a healthcare team to prevent complications and improve quality of life for patients.

The exact cause of polycythemia vera is not known, but it is believed to be due to a genetic mutation in the JAK2 gene, which is involved in the signaling pathways that regulate blood cell production. The condition typically affects adults over the age of 60 and is more common in men than women.

Symptoms of polycythemia vera can include:

* Fatigue
* Weakness
* Shortness of breath
* Headaches
* Dizziness
* Itching
* Night sweats
* Weight loss

Diagnosis of polycythemia vera is typically made based on a combination of physical examination, medical history, and laboratory tests, including:

* Complete blood count (CBC) to measure the levels of red blood cells, white blood cells, and platelets
* Blood chemistry tests to assess liver function and other body chemicals
* Genetic testing to look for the JAK2 mutation
* Bone marrow biopsy to examine the bone marrow tissue for abnormalities

Treatment for polycythemia vera usually involves phlebotomy (the removal of blood from the body) to reduce the number of red blood cells and relieve symptoms such as itching and night sweats. In some cases, medications may be used to reduce the production of blood cells or to treat specific symptoms. Regular monitoring by a healthcare provider is important to detect any changes in the condition and to prevent complications.

Overall, polycythemia vera is a chronic and progressive disease that can have significant impact on quality of life if left untreated. Early diagnosis and appropriate treatment can help manage symptoms and improve outcomes for patients with this condition.

Some examples of pathologic constrictions include:

1. Stenosis: A narrowing or constriction of a blood vessel or other tubular structure, often caused by the buildup of plaque or scar tissue.
2. Asthma: A condition characterized by inflammation and constriction of the airways, which can make breathing difficult.
3. Esophageal stricture: A narrowing of the esophagus that can cause difficulty swallowing.
4. Gastric ring constriction: A narrowing of the stomach caused by a band of tissue that forms in the upper part of the stomach.
5. Anal fissure: A tear in the lining of the anus that can cause pain and difficulty passing stools.

Pathologic constrictions can be caused by a variety of factors, including inflammation, infection, injury, or genetic disorders. They can be diagnosed through imaging tests such as X-rays, CT scans, or endoscopies, and may require surgical treatment to relieve symptoms and improve function.

Some common puerperal disorders include:

1. Puerperal fever: This is a bacterial infection that can occur during the postpartum period, usually caused by Streptococcus or Staphylococcus bacteria. Symptoms include fever, chills, and abdominal pain.
2. Postpartum endometritis: This is an inflammation of the lining of the uterus that can occur after childbirth, often caused by bacterial infection. Symptoms include fever, abdominal pain, and vaginal discharge.
3. Postpartum bleeding: This is excessive bleeding that can occur during the postpartum period, often caused by tears or lacerations to the uterus or cervix during childbirth.
4. Breast engorgement: This is a common condition that occurs when the breasts become full and painful due to milk production.
5. Mastitis: This is an inflammation of the breast tissue that can occur during breastfeeding, often caused by bacterial infection. Symptoms include redness, swelling, and warmth in the breast.
6. Postpartum depression: This is a mood disorder that can occur after childbirth, characterized by feelings of sadness, anxiety, and hopelessness.
7. Postpartum anxiety: This is an anxiety disorder that can occur after childbirth, characterized by excessive worry, fear, and anxiety.
8. Urinary incontinence: This is the loss of bladder control during the postpartum period, often caused by weakened pelvic muscles.
9. Constipation: This is a common condition that can occur after childbirth, often caused by hormonal changes and decreased bowel motility.
10. Breastfeeding difficulties: These can include difficulty latching, painful feeding, and low milk supply.

It's important to note that not all women will experience these complications, and some may have different symptoms or none at all. Additionally, some complications may require medical attention, while others may be managed with self-care measures or support from a healthcare provider. It's important for new mothers to seek medical advice if they have any concerns about their physical or emotional well-being during the postpartum period.

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.

There are several types of aneurysms, including:

1. Thoracic aneurysm: This type of aneurysm occurs in the chest cavity and is usually caused by atherosclerosis or other conditions that affect the aorta.
2. Abdominal aneurysm: This type of aneurysm occurs in the abdomen and is usually caused by high blood pressure or atherosclerosis.
3. Cerebral aneurysm: This type of aneurysm occurs in the brain and can cause symptoms such as headaches, seizures, and stroke.
4. Peripheral aneurysm: This type of aneurysm occurs in the peripheral arteries, which are the blood vessels that carry blood to the arms and legs.

Symptoms of an aneurysm can include:

1. Pain or discomfort in the affected area
2. Swelling or bulging of the affected area
3. Weakness or numbness in the affected limb
4. Shortness of breath or chest pain (in the case of a thoracic aneurysm)
5. Headaches, seizures, or stroke (in the case of a cerebral aneurysm)

If an aneurysm is not treated, it can lead to serious complications such as:

1. Rupture: This is the most serious complication of an aneurysm and occurs when the aneurysm sac bursts, leading to severe bleeding and potentially life-threatening consequences.
2. Stroke or brain damage: If a cerebral aneurysm ruptures, it can cause a stroke or brain damage.
3. Infection: An aneurysm can become infected, which can lead to serious health problems.
4. Blood clots: An aneurysm can form blood clots, which can break loose and travel to other parts of the body, causing blockages or further complications.
5. Kidney failure: If an aneurysm is not treated, it can cause kidney failure due to the pressure on the renal arteries.
6. Heart problems: An aneurysm in the aorta can lead to heart problems such as heart failure or cardiac arrest.
7. Sepsis: If an aneurysm becomes infected, it can lead to sepsis, which is a life-threatening condition that can cause organ failure and death.

Treatment options for an aneurysm include:

1. Observation: Small aneurysms that are not causing any symptoms may not require immediate treatment and can be monitored with regular check-ups to see if they are growing or changing.
2. Surgery: Open surgery or endovascular repair are two common methods for treating aneurysms. In open surgery, the surgeon makes an incision in the abdomen to repair the aneurysm. In endovascular repair, a small tube is inserted into the affected blood vessel through an incision in the groin, and then guided to the site of the aneurysm where it is expanded to fill the aneurysm sac and seal off the aneurysm.
3. Embolization: This is a minimally invasive procedure where a small catheter is inserted into the affected blood vessel through an incision in the groin, and then guided to the site of the aneurysm where it releases tiny particles or coils that fill the aneurysm sac and seal off the aneurysm.
4. Medications: Certain medications such as antibiotics and blood thinners may be prescribed to treat related complications such as infection or blood clots.

It is important to seek medical attention if you experience any symptoms of an aneurysm, such as sudden severe headache, vision changes, difficulty speaking, weakness or numbness in the face or limbs, as prompt treatment can help prevent complications and improve outcomes.

In healthy individuals, the normal platelet count ranges from 150,000 to 450,000 platelets per microliter of blood. In thrombocytosis, the platelet count is significantly higher than this range, often above 600,000 platelets/μL.

Thrombocytosis can be caused by a variety of factors, including:

1. Bone marrow disorders: Disorders such as essential thrombocythemia, polycythemia vera, and myelofibrosis can lead to an overproduction of platelets in the bone marrow.
2. Infection: Sepsis and other infections can cause a temporary increase in platelet production.
3. Inflammation: Certain inflammatory conditions, such as appendicitis and pancreatitis, can also lead to thrombocytosis.
4. Cancer: Some types of cancer, such as leukemia and lymphoma, can cause an overproduction of platelets.
5. Medications: Certain medications, such as estrogens and corticosteroids, can increase platelet production.

Thrombocytosis can lead to a range of complications, including:

1. Blood clots: The excessive number of platelets in the blood can increase the risk of blood clots forming in the veins and arteries.
2. Pulmonary embolism: If a blood clot forms in the lungs, it can cause a pulmonary embolism, which can be life-threatening.
3. Stroke: Thrombocytosis can increase the risk of stroke, especially if there are existing risk factors such as high blood pressure or a history of cardiovascular disease.
4. Heart attack and heart failure: Excessive platelet activity can increase the risk of heart attack and heart failure.
5. Gastrointestinal bleeding: The increased number of platelets in the blood can make it more difficult to control bleeding, especially in the gastrointestinal tract.

Thrombocytosis is typically diagnosed through a combination of physical examination, medical history, and laboratory tests, such as:

1. Complete blood count (CBC): This test measures the number of platelets in the blood, as well as other components such as red and white blood cells.
2. Blood smear: A sample of blood is examined under a microscope to assess the shape and size of the platelets.
3. Bone marrow aspiration and biopsy: These tests involve removing a small sample of bone marrow tissue to examine the number and type of cells present.
4. Imaging studies: Imaging tests such as ultrasound, computed tomography (CT), or magnetic resonance imaging (MRI) may be used to look for evidence of blood clots or other complications.

Treatment for thrombocytosis depends on the underlying cause and the severity of the condition. Some common treatments include:

1. Medications: Drugs such as aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs), and blood thinners may be used to reduce the risk of blood clots and other complications.
2. Plateletpheresis: This is a procedure in which the patient's blood is removed and the platelets are separated from the rest of the blood components. The remaining blood is then returned to the body.
3. Splenectomy: In some cases, surgical removal of the spleen may be necessary to treat thrombocytosis.
4. Chemotherapy: This is a treatment that uses drugs to kill cancer cells, which can cause thrombocytosis in some cases.

Overall, it is important to seek medical attention if you experience any symptoms of thrombocytosis, as early diagnosis and treatment can help prevent complications and improve outcomes.

There are several types of inherited blood coagulation disorders, including:

1. Hemophilia A and B: These are the most common types of inherited bleeding disorders, caused by deficiencies in clotting factor VIII or IX, respectively.
2. Von Willebrand disease: This is a mild bleeding disorder caused by a deficiency in von Willebrand factor, a protein that helps platelets stick together to form blood clots.
3. Platelet function disorders: These are rare disorders caused by mutations in genes that code for proteins involved in platelet function, leading to impaired platelet aggregation and bleeding.
4. Factor V Leiden and prothrombin gene mutations: These are inherited disorders caused by mutations in the genes that code for clotting factors V and II, respectively.
5. Antiphospholipid syndrome: This is an autoimmune disorder that causes blood clots and bleeding, often in association with other symptoms such as joint pain and swelling.

Inherited blood coagulation disorders can cause a range of symptoms, including easy bruising, petechiae (small red spots on the skin), purpura (larger red or purple spots on the skin), and prolonged bleeding after injury or surgery. Treatment options vary depending on the specific disorder and severity of symptoms, and may include clotting factor replacement therapy, medications to improve platelet function, and lifestyle modifications such as avoiding certain medications and taking precautions during surgical procedures.

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.

The buildup of plaque in the coronary arteries is often caused by high levels of low-density lipoprotein (LDL) cholesterol, smoking, high blood pressure, diabetes, and a family history of heart disease. The plaque can also rupture, causing a blood clot to form, which can completely block the flow of blood to the heart muscle, leading to a heart attack.

CAD is the most common type of heart disease and is often asymptomatic until a serious event occurs. Risk factors for CAD include:

* Age (men over 45 and women over 55)
* Gender (men are at greater risk than women, but women are more likely to die from CAD)
* Family history of heart disease
* High blood pressure
* High cholesterol
* Diabetes
* Smoking
* Obesity
* Lack of exercise

Diagnosis of CAD typically involves a physical exam, medical history, and results of diagnostic tests such as:

* Electrocardiogram (ECG or EKG)
* Stress test
* Echocardiogram
* Coronary angiography

Treatment for CAD may include lifestyle changes such as a healthy diet, regular exercise, stress management, and quitting smoking. Medications such as beta blockers, ACE inhibitors, and statins may also be prescribed to manage symptoms and slow the progression of the disease. In severe cases, surgical intervention such as coronary artery bypass grafting (CABG) or percutaneous coronary intervention (PCI) may be necessary.

Prevention of CAD includes managing risk factors such as high blood pressure, high cholesterol, and diabetes, quitting smoking, maintaining a healthy weight, and getting regular exercise. Early detection and treatment of CAD can help to reduce the risk of complications and improve quality of life for those affected by the disease.

The term "infarction" is derived from the Latin words "in" meaning "into" and "farcire" meaning "to stuff", which refers to the idea that the tissue becomes "stuffed" with blood, leading to cell death and necrosis.

Infarction can be caused by a variety of factors, including atherosclerosis (the buildup of plaque in the blood vessels), embolism (a blood clot or other foreign material that blocks the flow of blood), and vasospasm (constriction of the blood vessels).

The symptoms of infarction vary depending on the location and severity of the blockage, but can include chest pain or discomfort, shortness of breath, numbness or weakness in the affected limbs, and confusion or difficulty speaking or understanding speech.

Diagnosis of infarction typically involves imaging tests such as electrocardiograms (ECGs), echocardiograms, or computerized tomography (CT) scans to confirm the presence of a blockage and assess the extent of the damage. Treatment options for infarction include medications to dissolve blood clots, surgery to restore blood flow, and other interventions to manage symptoms and prevent complications.

Prevention of infarction involves managing risk factors such as high blood pressure, high cholesterol, smoking, and obesity, as well as maintaining a healthy diet and exercise routine. Early detection and treatment of blockages can help reduce the risk of infarction and minimize the damage to affected tissues.

There are several types of embolism and thrombosis, including:

1. Pulmonary embolism: A blood clot that forms in the lungs and blocks the flow of blood to the heart.
2. Deep vein thrombosis (DVT): A blood clot that forms in the deep veins of the legs or arms and can break loose and travel to other parts of the body, causing embolism.
3. Cerebral embolism: A blood clot that forms in the brain and blocks the flow of blood to certain areas, which can cause a stroke or other neurological problems.
4. Gastrointestinal embolism: A blood clot that forms in the digestive tract and blocks the flow of blood to certain organs, such as the liver or intestines.
5. Hepatic embolism: A blood clot that forms in the liver and blocks the flow of blood to other parts of the body.
6. Renal embolism: A blood clot that forms in the kidneys and blocks the flow of blood to other organs, such as the heart or brain.
7. Arterial embolism: A blood clot that forms in an artery and blocks the flow of blood to certain areas of the body.

Embolism and thrombosis can be caused by a variety of factors, including genetics, injury, surgery, infection, and certain medical conditions, such as atrial fibrillation or cancer. Treatment options for embolism and thrombosis depend on the underlying cause and the severity of the condition, but may include medications to dissolve blood clots, surgery to remove clots, or other interventional procedures to restore blood flow.

There are several risk factors for developing venous insufficiency, including:

* Age: As we age, our veins become less effective at pumping blood back to the heart, making us more susceptible to venous insufficiency.
* Gender: Women are more likely to develop venous insufficiency than men due to hormonal changes and other factors.
* Family history: If you have a family history of venous insufficiency, you may be more likely to develop the condition.
* Injury or trauma: Injuries or traumas to the veins can damage valves or cause blood clots, leading to venous insufficiency.
* Obesity: Excess weight can put extra pressure on the veins, increasing the risk of venous insufficiency.

Symptoms of venous insufficiency may include:

* Pain, aching, or cramping in the legs
* Swelling, edema, or water retention in the legs
* Skin discoloration or thickening of the skin on the legs
* Itching or burning sensations on the skin
* Ulcers or sores on the skin

If left untreated, venous insufficiency can lead to more serious complications such as:

* Chronic wounds or ulcers
* Blood clots or deep vein thrombosis (DVT)
* Increased risk of infection
* Decreased mobility and quality of life

To diagnose venous insufficiency, a healthcare provider may perform one or more of the following tests:

* Physical examination: A healthcare provider will typically examine the legs and ankles to check for swelling, discoloration, and other symptoms.
* Duplex ultrasound: This non-invasive test uses sound waves to evaluate blood flow in the veins and can detect blockages or other problems.
* Venography: This test involves injecting a dye into the vein to visualize the veins and check for any blockages or abnormalities.
* Imaging tests: Such as MRI, CT scan, or X-rays may be used to rule out other conditions that may cause similar symptoms.

Treatment options for venous insufficiency depend on the underlying cause and severity of the condition, but may include one or more of the following:

* Compression stockings: These specialized stockings provide gentle pressure to the legs and ankles to help improve blood flow and reduce swelling.
* Lifestyle changes: Maintaining a healthy weight, exercising regularly, and avoiding prolonged standing or sitting can help improve symptoms.
* Medications: Such as diuretics, anticoagulants, or pain relievers may be prescribed to manage symptoms and prevent complications.
* Endovenous laser therapy: This minimally invasive procedure uses a laser to heat and seal off the damaged vein, redirecting blood flow to healthier veins.
* Sclerotherapy: This involves injecting a solution into the affected vein to cause it to collapse and be absorbed by the body.
* Vein stripping: In this surgical procedure, the affected vein is removed through small incisions.

It's important to note that these treatments are usually recommended for more severe cases of venous insufficiency, and for those who have not responded well to other forms of treatment. Your healthcare provider will help determine the best course of treatment for your specific case.

Note: Portal hypertension is a common complication of liver disease, especially cirrhosis. It is characterized by elevated pressure within the portal vein system, which can lead to splanchnic vasodilation, increased blood flow, and edema in the splanchnic organ.

Symptoms: Symptoms of portal hypertension may include ascites (fluid accumulation in the abdomen), encephalopathy (mental confusion or disorientation), gastrointestinal bleeding, and jaundice (yellowing of the skin and eyes).

Diagnosis: The diagnosis of portal hypertension is based on a combination of clinical findings, laboratory tests, and imaging studies. Laboratory tests may include liver function tests, blood counts, and coagulation studies. Imaging studies may include ultrasonography, computed tomography (CT), or magnetic resonance imaging (MRI).

Treatment: Treatment of portal hypertension depends on the underlying cause and may include medications to control symptoms, such as beta blockers to reduce portal pressure, antibiotics to treat infection, and nonsteroidal anti-inflammatory drugs (NSAIDs) to relieve pain. In severe cases, surgery or shunt procedures may be necessary.

Prognosis: The prognosis for patients with portal hypertension is generally poor, as it is often associated with advanced liver disease. The 5-year survival rate for patients with cirrhosis and portal hypertension is approximately 50%.

It is important to identify and address prosthesis failure early to prevent further complications and restore the functionality of the device. This may involve repairing or replacing the device, modifying the design, or changing the materials used in its construction. In some cases, surgical intervention may be necessary to correct issues related to the implantation of the prosthetic device.

Prosthesis failure can occur in various types of prosthetic devices, including joint replacements, dental implants, and orthotic devices. The causes of prosthesis failure can range from manufacturing defects to user error or improper maintenance. It is essential to have a comprehensive understanding of the factors contributing to prosthesis failure to develop effective solutions and improve patient outcomes.

In conclusion, prosthesis failure is a common issue that can significantly impact the quality of life of individuals who rely on prosthetic devices. Early identification and addressing of prosthesis failure are crucial to prevent further complications and restore functionality. A comprehensive understanding of the causes of prosthesis failure is necessary to develop effective solutions and improve patient outcomes.

Causes:

Factor XII deficiency can be acquired or inherited. Acquired factor XII deficiency can occur due to autoantibodies, liver disease, or vitamin K deficiency. Inherited factor XII deficiency is caused by mutations in the F12 gene, which is responsible for producing factor XII.

Symptoms:

People with factor XII deficiency may experience recurring bleeding episodes, especially after injury or surgery. The bleeding can be severe and may occur spontaneously without any apparent cause. Other symptoms include easy bruising, petechiae (small red or purple spots on the skin), and nosebleeds.

Diagnosis:

Factor XII deficiency is diagnosed through blood tests that measure the levels of factor XII in the blood. A low level of factor XII indicates a deficiency. Other tests, such as a platelet aggregation test or a bleeding time test, may also be performed to assess the severity of the condition.

Treatment:

Treatment for factor XII deficiency typically involves replacing the missing factor XII with infusions of the protein. This can be done on an as-needed basis or regularly, depending on the severity of the condition. Desmopressin, a hormone that stimulates the release of von Willebrand factor and platelets, may also be used to treat mild cases of factor XII deficiency. In severe cases, surgery may be necessary to repair damaged blood vessels or organs.

Prognosis:

The prognosis for factor XII deficiency is generally good if the condition is properly treated. With regular infusions of factor XII and proper management, most people with the condition can lead normal lives and avoid complications. However, untreated factor XII deficiency can lead to serious complications, such as bleeding or organ damage, which can be life-threatening.

Lifestyle Changes:

There are no specific lifestyle changes that can cure factor XII deficiency, but certain lifestyle modifications may help manage the condition. These include avoiding activities that could trigger bleeding, taking regular breaks to rest and elevate the affected limb, and avoiding alcohol and other drugs that can exacerbate the condition.

Alternative Treatments:

There are no alternative treatments for factor XII deficiency, as infusions of the protein are the only effective way to manage the condition. However, some complementary therapies, such as acupuncture or herbal supplements, may help reduce symptoms and improve quality of life.

Prevention:

Factor XII deficiency cannot be prevented, as it is an inherited condition. However, early diagnosis and proper management can help prevent complications and ensure a good prognosis. Pregnant women with a history of factor XII deficiency should receive regular prenatal care to monitor the health of their baby.

Living With Factor XII Deficiency:

Living with factor XII deficiency can be challenging, as it can impact daily life and increase the risk of bleeding. However, with proper management and support, people with this condition can lead fulfilling lives. It is essential to work closely with a healthcare provider to develop a personalized treatment plan and make necessary lifestyle adjustments.

Prognosis:

The prognosis for factor XII deficiency is generally good if the condition is properly managed. With regular infusions of the protein, most people with this condition can lead normal lives and avoid serious complications. However, in some cases, the condition may progress to more severe bleeding episodes or other complications, which can be life-threatening.

In conclusion, factor XII deficiency is a rare genetic disorder that can cause excessive bleeding due to a lack of a critical blood clotting protein. While there is no cure for the condition, infusions of the protein can help manage symptoms and prevent complications. Early diagnosis and proper management are essential to ensure a good prognosis and improve quality of life for those affected by this condition.

A sudden and unexpected tearing or breaking open of a bodily structure, such as a blood vessel, muscle, or tendon, without any obvious external cause. This can occur due to various factors, including genetic predisposition, aging, or other underlying medical conditions.

Examples:

* Spontaneous rupture of the Achilles tendon
* Spontaneous coronary artery dissection (SCAD)
* Spontaneous pneumothorax (collapsed lung)

Symptoms and Signs:

* Sudden, severe pain
* Swelling and bruising in the affected area
* Difficulty moving or using the affected limb
* Palpitations or shortness of breath (in cardiac cases)

Diagnosis:

* Physical examination and medical history
* Imaging tests, such as X-rays, CT scans, or MRI scans, to confirm the rupture and assess the extent of damage
* Blood tests to check for underlying conditions that may have contributed to the rupture

Treatment:

* Rest, ice, compression, and elevation (RICE) to reduce pain and swelling
* Immobilization of the affected limb with a cast or brace
* Medications to manage pain and inflammation
* Surgery may be required in some cases to repair the damaged tissue or organ

Prognosis:

* The prognosis for spontaneous rupture depends on the location and severity of the rupture, as well as the underlying cause. In general, the sooner treatment is received, the better the outcome.

Complications:

* Infection
* Further damage to surrounding tissues or organs
* Chronic pain or limited mobility
* In some cases, long-term disability or death

The severity of coronary stenosis can range from mild to severe, with blockages ranging from 15% to over 90%. In mild cases, lifestyle changes and medication may be enough to manage symptoms. However, more severe cases typically require interventional procedures such as angioplasty or bypass surgery to improve blood flow to the heart.

The syndrome can be caused by a variety of factors, including:

* Compression from a tumor or other mass in the chest or neck
* Injury to the vein from trauma or surgery
* Blood clots or thrombophlebitis (inflammation of the vein wall)
* Infection or inflammation of the vein
* Cardiac tamponade (fluid accumulation in the pericardial sac surrounding the heart)

Symptoms of SVC syndrome can vary depending on the location and severity of the compression. They may include:

* Swelling of the face, neck, and arms
* Shortness of breath
* Difficulty speaking or swallowing
* Pain in the head, neck, or chest
* Fatigue or weakness
* Decreased consciousness or confusion

If you suspect that you or someone else may be experiencing SVC syndrome, it is important to seek medical attention immediately. A healthcare provider will perform a physical examination and order diagnostic tests, such as imaging studies or blood tests, to determine the cause of the symptoms and develop an appropriate treatment plan.

Treatment for SVC syndrome may include:

* Anticoagulation medications to prevent blood clots from forming
* Pain management medications to relieve swelling and discomfort
* Surgery to remove a tumor or other mass compressing the vein
* Endovascular procedures, such as angioplasty or stenting, to open up the vein and restore blood flow
* Supportive care, such as oxygen therapy or mechanical ventilation, in severe cases.

Early diagnosis and treatment are critical to prevent complications and improve outcomes for patients with SVC syndrome. If you suspect that you or someone else may be experiencing symptoms of this condition, do not hesitate to seek medical attention right away.

There are several factors that can contribute to hyperhomocysteinemia, including:

1. Genetic mutations: Some individuals may have genetic mutations that affect the enzymes involved in homocysteine metabolism, leading to elevated levels of homocysteine.
2. Vitamin deficiencies: Deficiencies in vitamins B6, B12, and folate can interfere with the metabolism of homocysteine, leading to elevated levels.
3. Kidney disease: The kidneys play a critical role in removing homocysteine from the body. Any damage to the kidneys or impairment in their function can lead to hyperhomocysteinemia.
4. Other medical conditions: Certain medical conditions, such as thyroid disorders and autoimmune diseases, can also contribute to hyperhomocysteinemia.

Elevated levels of homocysteine have been linked to several health problems, including:

1. Cardiovascular disease: High levels of homocysteine have been associated with an increased risk of heart disease and stroke.
2. Blood clots: Homocysteine can interfere with the normal blood clotting process, leading to an increased risk of blood clots and deep vein thrombosis.
3. Bone loss: Elevated levels of homocysteine have been linked to bone loss and an increased risk of osteoporosis.
4. Cognitive decline: Some studies suggest that high levels of homocysteine may be associated with cognitive decline and an increased risk of dementia.

Treatment for hyperhomocysteinemia typically involves addressing any underlying medical conditions, such as kidney disease or thyroid disorders, and making dietary changes to increase the intake of vitamin B6, folate, and other nutrients that help regulate homocysteine levels. In some cases, medications may be prescribed to lower homocysteine levels. Regular monitoring of homocysteine levels can help healthcare providers track the effectiveness of treatment and make any necessary adjustments.

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.

1. Atherosclerosis: A condition in which plaque builds up inside the arteries, causing them to narrow and harden. This can lead to heart disease, heart attack, or stroke.
2. Hypertension: High blood pressure that can damage blood vessels and increase the risk of heart disease, stroke, and other conditions.
3. Peripheral artery disease (PAD): A condition in which the blood vessels in the legs and arms become narrowed or blocked, leading to pain, cramping, and weakness in the affected limbs.
4. Raynaud's phenomenon: A condition that causes blood vessels in the hands and feet to constrict in response to cold temperatures or stress, leading to discoloration, numbness, and tissue damage.
5. Deep vein thrombosis (DVT): A condition in which a blood clot forms in the deep veins of the legs, often caused by immobility or injury.
6. Varicose veins: Enlarged, twisted veins that can cause pain, swelling, and cosmetic concerns.
7. Angioplasty: A medical procedure in which a balloon is used to open up narrowed blood vessels, often performed to treat peripheral artery disease or blockages in the legs.
8. Stenting: A medical procedure in which a small mesh tube is placed inside a blood vessel to keep it open and improve blood flow.
9. Carotid endarterectomy: A surgical procedure to remove plaque from the carotid arteries, which supply blood to the brain, to reduce the risk of stroke.
10. Bypass surgery: A surgical procedure in which a healthy blood vessel is used to bypass a blocked or narrowed blood vessel, often performed to treat coronary artery disease or peripheral artery disease.

Overall, vascular diseases can have a significant impact on quality of life and can increase the risk of serious complications such as stroke, heart attack, and amputation. It is important to seek medical attention if symptoms persist or worsen over time, as early diagnosis and treatment can help to prevent long-term damage and improve outcomes.

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.

Coronary disease is often caused by a combination of genetic and lifestyle factors, such as high blood pressure, high cholesterol levels, smoking, obesity, and a lack of physical activity. It can also be triggered by other medical conditions, such as diabetes and kidney disease.

The symptoms of coronary disease can vary depending on the severity of the condition, but may include:

* Chest pain or discomfort (angina)
* Shortness of breath
* Fatigue
* Swelling of the legs and feet
* Pain in the arms and back

Coronary disease is typically diagnosed through a combination of physical examination, medical history, and diagnostic tests such as electrocardiograms (ECGs), stress tests, and cardiac imaging. Treatment for coronary disease may include lifestyle changes, medications to control symptoms, and surgical procedures such as angioplasty or bypass surgery to improve blood flow to the heart.

Preventative measures for coronary disease include:

* Maintaining a healthy diet and exercise routine
* Quitting smoking and limiting alcohol consumption
* Managing high blood pressure, high cholesterol levels, and other underlying medical conditions
* Reducing stress through relaxation techniques or therapy.

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.

Cerebral infarction can result in a range of symptoms, including sudden weakness or numbness in the face, arm, or leg on one side of the body, difficulty speaking or understanding speech, sudden vision loss, dizziness, and confusion. Depending on the location and severity of the infarction, it can lead to long-term disability or even death.

There are several types of cerebral infarction, including:

1. Ischemic stroke: This is the most common type of cerebral infarction, accounting for around 87% of all cases. It occurs when a blood clot blocks the flow of blood to the brain, leading to cell death and tissue damage.
2. Hemorrhagic stroke: This type of cerebral infarction occurs when a blood vessel in the brain ruptures, leading to bleeding and cell death.
3. Lacunar infarction: This type of cerebral infarction affects the deep structures of the brain, particularly the basal ganglia, and is often caused by small blockages or stenosis (narrowing) in the blood vessels.
4. Territorial infarction: This type of cerebral infarction occurs when there is a complete blockage of a blood vessel that supplies a specific area of the brain, leading to cell death and tissue damage in that area.

Diagnosis of cerebral infarction typically involves a combination of physical examination, medical history, and imaging tests such as CT or MRI scans. Treatment options vary depending on the cause and location of the infarction, but may include medication to dissolve blood clots, surgery to remove blockages, or supportive care to manage symptoms and prevent complications.

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.

Arteriosclerosis can affect any artery in the body, but it is most commonly seen in the arteries of the heart, brain, and legs. It is a common condition that affects millions of people worldwide and is often associated with aging and other factors such as high blood pressure, high cholesterol, diabetes, and smoking.

There are several types of arteriosclerosis, including:

1. Atherosclerosis: This is the most common type of arteriosclerosis and occurs when plaque builds up inside the arteries.
2. Arteriolosclerosis: This type affects the small arteries in the body and can cause decreased blood flow to organs such as the kidneys and brain.
3. Medial sclerosis: This type affects the middle layer of the artery wall and can cause stiffness and narrowing of the arteries.
4. Intimal sclerosis: This type occurs when plaque builds up inside the innermost layer of the artery wall, causing it to become thick and less flexible.

Symptoms of arteriosclerosis can include chest pain, shortness of breath, leg pain or cramping during exercise, and numbness or weakness in the limbs. Treatment for arteriosclerosis may include lifestyle changes such as a healthy diet and regular exercise, as well as medications to lower blood pressure and cholesterol levels. In severe cases, surgery may be necessary to open up or bypass blocked arteries.

The thoracic outlet is a narrow passageway between the scalene muscles and the first and second ribs. It contains several important structures, including the brachial plexus nerves, the subclavian artery and vein, and the phrenic nerve. When these structures are compressed or irritated, it can cause symptoms in the arm and hand.

TOS is relatively rare, but it can be caused by a variety of factors, including:

1. Congenital defects, such as a narrow thoracic outlet or abnormal development of the rib cage.
2. Trauma, such as a fall onto the shoulder or a direct blow to the chest.
3. Repetitive movements, such as typing or using a computer mouse.
4. Poor posture or body mechanics.
5. Muscle imbalances or weakness in the neck and shoulder muscles.
6. Ganglion cysts or other soft tissue masses that compress the nerves or blood vessels.
7. Fractures or dislocations of the clavicle or shoulder blade.
8. Tumors or other abnormal growths in the chest or neck.
9. Inflammatory conditions, such as rheumatoid arthritis or thyroiditis.

Symptoms of TOS can vary depending on the location and severity of the compression. They may include:

1. Pain in the shoulder or arm, which can be exacerbated by movement or activity.
2. Numbness, tingling, or weakness in the hand or fingers.
3. Difficulty coordinating movements or performing fine motor tasks.
4. Weakness or fatigue in the muscles of the shoulder and arm.
5. Decreased grip strength or dexterity.
6. Pain or tingling that radiates down the arm or into the hand.
7. Swelling or redness in the neck or shoulder.
8. Difficulty swallowing or breathing, in severe cases.

TOS can be difficult to diagnose, as the symptoms can be similar to those of other conditions such as carpal tunnel syndrome or a heart attack. A thorough physical examination and medical history are important for making an accurate diagnosis. Imaging studies such as X-rays, CT scans, or MRI may also be used to help identify any underlying structural abnormalities or nerve compression. Electromyography (EMG) and nerve conduction studies (NCS) may also be performed to assess nerve function and determine the extent of nerve damage.

Treatment for TOS depends on the underlying cause and severity of the condition. Conservative treatments may include:

1. Rest and avoidance of activities that exacerbate the symptoms.
2. Physical therapy to improve posture, strength, and range of motion.
3. Anti-inflammatory medications or pain relievers to reduce swelling and relieve pain.
4. Muscle relaxants to reduce muscle spasm and tension.
5. Injections of steroids or local anesthetics to reduce inflammation and relieve pain.
6. Surgery may be necessary in severe cases, such as when there is significant nerve compression or instability of the shoulder joint.

It's important to seek medical attention if you experience any symptoms of TOS, as early diagnosis and treatment can help prevent long-term complications and improve 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.

There are several types of ischemia, including:

1. Myocardial ischemia: Reduced blood flow to the heart muscle, which can lead to chest pain or a heart attack.
2. Cerebral ischemia: Reduced blood flow to the brain, which can lead to stroke or cognitive impairment.
3. Peripheral arterial ischemia: Reduced blood flow to the legs and arms.
4. Renal ischemia: Reduced blood flow to the kidneys.
5. Hepatic ischemia: Reduced blood flow to the liver.

Ischemia can be diagnosed through a variety of tests, including electrocardiograms (ECGs), stress tests, and imaging studies such as CT or MRI scans. Treatment for ischemia depends on the underlying cause and may include medications, lifestyle changes, or surgical interventions.

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.

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.

Neoplasm refers to an abnormal growth of cells that can be benign (non-cancerous) or malignant (cancerous). Neoplasms can occur in any part of the body and can affect various organs and tissues. The term "neoplasm" is often used interchangeably with "tumor," but while all tumors are neoplasms, not all neoplasms are tumors.

Types of Neoplasms

There are many different types of neoplasms, including:

1. Carcinomas: These are malignant tumors that arise in the epithelial cells lining organs and glands. Examples include breast cancer, lung cancer, and colon cancer.
2. Sarcomas: These are malignant tumors that arise in connective tissue, such as bone, cartilage, and fat. Examples include osteosarcoma (bone cancer) and soft tissue sarcoma.
3. Lymphomas: These are cancers of the immune system, specifically affecting the lymph nodes and other lymphoid tissues. Examples include Hodgkin lymphoma and non-Hodgkin lymphoma.
4. Leukemias: These are cancers of the blood and bone marrow that affect the white blood cells. Examples include acute myeloid leukemia (AML) and chronic lymphocytic leukemia (CLL).
5. Melanomas: These are malignant tumors that arise in the pigment-producing cells called melanocytes. Examples include skin melanoma and eye melanoma.

Causes and Risk Factors of Neoplasms

The exact causes of neoplasms are not fully understood, but there are several known risk factors that can increase the likelihood of developing a neoplasm. These include:

1. Genetic predisposition: Some people may be born with genetic mutations that increase their risk of developing certain types of neoplasms.
2. Environmental factors: Exposure to certain environmental toxins, such as radiation and certain chemicals, can increase the risk of developing a neoplasm.
3. Infection: Some neoplasms are caused by viruses or bacteria. For example, human papillomavirus (HPV) is a common cause of cervical cancer.
4. Lifestyle factors: Factors such as smoking, excessive alcohol consumption, and a poor diet can increase the risk of developing certain types of neoplasms.
5. Family history: A person's risk of developing a neoplasm may be higher if they have a family history of the condition.

Signs and Symptoms of Neoplasms

The signs and symptoms of neoplasms can vary depending on the type of cancer and where it is located in the body. Some common signs and symptoms include:

1. Unusual lumps or swelling
2. Pain
3. Fatigue
4. Weight loss
5. Change in bowel or bladder habits
6. Unexplained bleeding
7. Coughing up blood
8. Hoarseness or a persistent cough
9. Changes in appetite or digestion
10. Skin changes, such as a new mole or a change in the size or color of an existing mole.

Diagnosis and Treatment of Neoplasms

The diagnosis of a neoplasm usually involves a combination of physical examination, imaging tests (such as X-rays, CT scans, or MRI scans), and biopsy. A biopsy involves removing a small sample of tissue from the suspected tumor and examining it under a microscope for cancer cells.

The treatment of neoplasms depends on the type, size, location, and stage of the cancer, as well as the patient's overall health. Some common treatments include:

1. Surgery: Removing the tumor and surrounding tissue can be an effective way to treat many types of cancer.
2. Chemotherapy: Using drugs to kill cancer cells can be effective for some types of cancer, especially if the cancer has spread to other parts of the body.
3. Radiation therapy: Using high-energy radiation to kill cancer cells can be effective for some types of cancer, especially if the cancer is located in a specific area of the body.
4. Immunotherapy: Boosting the body's immune system to fight cancer can be an effective treatment for some types of cancer.
5. Targeted therapy: Using drugs or other substances to target specific molecules on cancer cells can be an effective treatment for some types of cancer.

Prevention of Neoplasms

While it is not always possible to prevent neoplasms, there are several steps that can reduce the risk of developing cancer. These include:

1. Avoiding exposure to known carcinogens (such as tobacco smoke and radiation)
2. Maintaining a healthy diet and lifestyle
3. Getting regular exercise
4. Not smoking or using tobacco products
5. Limiting alcohol consumption
6. Getting vaccinated against certain viruses that are associated with cancer (such as human papillomavirus, or HPV)
7. Participating in screening programs for early detection of cancer (such as mammograms for breast cancer and colonoscopies for colon cancer)
8. Avoiding excessive exposure to sunlight and using protective measures such as sunscreen and hats to prevent skin cancer.

It's important to note that not all cancers can be prevented, and some may be caused by factors that are not yet understood or cannot be controlled. However, by taking these steps, individuals can reduce their risk of developing cancer and improve their overall health and well-being.

Example sentences for 'Aneurysm, False'

The patient was diagnosed with a false aneurysm after experiencing sudden severe pain in his leg following a fall.
The surgeon treated the false aneurysm by inserting a catheter into the affected blood vessel and using it to deliver a special coil that would seal off the dilated area.

Portal hypertension can be caused by several conditions, such as cirrhosis (scarring of the liver), liver cancer, and congenital heart disease. When the portal vein is blocked or narrowed, blood flow through the veins in the esophagus and stomach increases, leading to enlargement of these vessels and an increased risk of bleeding.

Esophageal varices are the most common type of variceal bleeding and account for about 75% of all cases. Gastric varices are less common and usually occur in conjunction with esophageal varices.

Symptoms of esophageal and gastric varices may include:

* Vomiting blood or passing black stools
* Weakness, dizziness, or fainting due to blood loss
* Chest pain or discomfort
* Difficulty swallowing

Treatment for esophageal and gastric varices usually involves endoscopy, which is a procedure in which a flexible tube with a camera and light on the end is inserted through the mouth to visualize the inside of the esophagus and stomach. During endoscopy, the physician may use medications to shrink the varices or apply heat to seal off the bleeding vessels. In some cases, surgery may be necessary to repair or remove the varices.

Prevention of esophageal and gastric varices involves managing the underlying cause of portal hypertension, such as cirrhosis or liver cancer. This can include medications to reduce portal pressure, lifestyle changes to improve liver function, and in some cases, surgery to remove the affected liver tissue.

In summary, esophageal and gastric varices are enlarged veins in the lower esophagus and stomach that can develop in people with portal hypertension due to cirrhosis or liver cancer. These varices can cause bleeding, which can be life-threatening if not treated promptly. Treatment usually involves endoscopy and may involve medications, heat therapy, or surgery to seal off the bleeding vessels. Prevention involves managing the underlying cause of portal hypertension.

There are several types of carotid artery injuries, including:

1. Carotid artery dissection: This is a tear in the inner lining of the artery that can lead to bleeding and inflammation.
2. Carotid artery thrombosis: This is the formation of a blood clot within the artery that can block blood flow to the brain.
3. Carotid artery occlusion: This is the complete blockage of the artery, which can cause a stroke or transient ischemic attack (TIA).
4. Carotid artery injury due to trauma: This type of injury can occur as a result of a blow to the neck or head.
5. Carotid artery injury due to surgery: This type of injury can occur during surgical procedures that involve the carotid arteries, such as endarterectomy or stenting.

The symptoms of carotid artery injuries can vary depending on the severity of the injury and the location of the damage. Some common symptoms include:

* Sudden weakness or numbness in the face, arm, or leg
* Sudden confusion or trouble speaking
* Sudden vision loss or double vision
* Sudden difficulty walking or maintaining balance
* Sudden severe headache

The diagnosis of carotid artery injuries is typically made using imaging tests such as ultrasound, computed tomography (CT) scans, or magnetic resonance imaging (MRI). Treatment options for carotid artery injuries depend on the severity and location of the injury, and may include medications, endovascular procedures, or surgery.

Prevention of carotid artery injuries is key to reducing the risk of complications. This can be achieved through:

* Maintaining a healthy lifestyle, including regular exercise and a balanced diet
* Avoiding smoking and limiting alcohol consumption
* Managing underlying medical conditions such as high blood pressure or diabetes
* Properly managing medications that may increase the risk of bleeding or injury
* Using appropriate precautions during surgical procedures, such as using sterile equipment and monitoring for signs of bleeding or injury.

In conclusion, carotid artery injuries can have serious consequences if left untreated. It is important to be aware of the causes, symptoms, diagnosis, and treatment options for these injuries in order to provide appropriate care and prevent complications. Proper precautions during surgical procedures and a healthy lifestyle can also help reduce the risk of carotid artery injuries.

Symptoms of Fusobacterium infections can vary depending on the location of the infection, but may include fever, chills, fatigue, and pain or swelling at the site of the infection. In severe cases, Fusobacterium infections can lead to life-threatening complications, such as sepsis or meningitis.

Diagnosis of a Fusobacterium infection typically involves a combination of physical examination, medical history, and laboratory tests, such as blood cultures or tissue samples. Treatment typically involves antibiotics, and the choice of antibiotic may depend on the severity and location of the infection, as well as the patient's underlying health conditions.

Prevention of Fusobacterium infections is challenging, but good hygiene practices, such as hand washing and proper wound care, can help reduce the risk of infection. In high-risk individuals, prophylactic antibiotics may be used to prevent infections in certain situations, such as before dental or surgical procedures.

Fusobacterium infections are a relatively rare but potentially serious condition that can affect people with weakened immune systems. Prompt diagnosis and appropriate treatment are essential to prevent complications and ensure a successful outcome.

The disorder is caused by mutations in the HBB gene that codes for the beta-globin subunit of hemoglobin. These mutations result in the production of abnormal hemoglobins that are unstable and prone to breakdown, leading to the release of free hemoglobin into the urine.

HP is classified into two types based on the severity of symptoms:

1. Type 1 HP: This is the most common form of the disorder and is characterized by mild to moderate anemia, occasional hemoglobinuria, and a normal life expectancy.
2. Type 2 HP: This is a more severe form of the disorder and is characterized by severe anemia, recurrent hemoglobinuria, and a shorter life expectancy.

There is no cure for HP, but treatment options are available to manage symptoms and prevent complications. These may include blood transfusions, folic acid supplements, and medications to reduce the frequency and severity of hemoglobinuria episodes.

Symptoms of intracranial hypertension can include headache, nausea and vomiting, confusion, seizures, and loss of consciousness. Treatment options depend on the underlying cause, but may include medications to reduce pressure, draining excess CSF, or surgery to relieve obstruction.

Intracranial hypertension can be life-threatening if left untreated, as it can lead to permanent brain damage and even death. Therefore, prompt medical attention is essential for proper diagnosis and management of this condition.

1. Aneurysms: A bulge or ballooning in the wall of the aorta that can lead to rupture and life-threatening bleeding.
2. Atherosclerosis: The buildup of plaque in the inner lining of the aorta, which can narrow the artery and restrict blood flow.
3. Dissections: A tear in the inner layer of the aortic wall that can cause bleeding and lead to an aneurysm.
4. Thoracic aortic disease: Conditions that affect the thoracic portion of the aorta, such as atherosclerosis or dissections.
5. Abdominal aortic aneurysms: Enlargement of the abdominal aorta that can lead to rupture and life-threatening bleeding.
6. Aortic stenosis: Narrowing of the aortic valve, which can impede blood flow from the heart into the aorta.
7. Aortic regurgitation: Backflow of blood from the aorta into the heart due to a faulty aortic valve.
8. Marfan syndrome: A genetic disorder that affects the body's connective tissue, including the aorta.
9. Ehlers-Danlos syndrome: A group of genetic disorders that affect the body's connective tissue, including the aorta.
10. Turner syndrome: A genetic disorder that affects females and can cause aortic diseases.

Aortic diseases can be diagnosed through imaging tests such as ultrasound, CT scan, or MRI. Treatment options vary depending on the specific condition and may include medication, surgery, or endovascular procedures.

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"Management of Pump Thrombosis in Patients with LVADs". "Management of Pump Thrombosis in Patients with LVADs". Blitz, A (2014 ... The occurrence of elevated LDH levels within 3 months after implantation mirrored that of thrombosis. Thrombosis was presaged ... Pump thrombosis is defined as a specific case of a major device malfunction. In turn, device malfunction is as defined by ... Pump thrombosis (PT) is considered a specific case of a major device malfunction, and is classified as either suspected or ...
Sexton, Travis; Smyth, Susan S. (January 2014). "Novel mediators and biomarkers of thrombosis". Journal of Thrombosis and ... Coronary thrombosis is defined as the formation of a blood clot inside a blood vessel of the heart. This blood clot may then ... Thrombosis is defined as the formation of a thrombus (blood clot) inside a blood vessel, leading to obstruction of blood flow ... Coronary thrombosis refers to the formation and presence of thrombi in the coronary arteries of the heart. Note that the heart ...
... is also recommended during air travel. Thrombosis prophylaxis is effective in preventing the formation of ... Thrombosis prevention or thromboprophylaxis is medical treatment to prevent the development of thrombosis (blood clots inside ... Thrombosis prophylaxis is not only used for the prevention of deep vein thrombosis, but can be initiated for the prevention of ... Thrombosis that develops into DVT will affect 900,000 people and kill up to 100,000 in the US. On average 28,726 hospitalized ...
... (previously known as 'Lifeblood, the Thrombosis Charity') is a UK based charity whose stated mission is to ... "Why Lifeblood: The Thrombosis Charity was founded". Lifeblood, the Thrombosis Charity. Archived from the original on 18 June ... Along with efforts to support research in thrombosis and to raise awareness through an annual "National Thrombosis Week", they ... improving medical and general knowledge of thrombosis, and raising funds for research into thrombosis. In 2003, the charity ...
... is an international peer-reviewed medical journal published by Elsevier with a goal of rapid dissemination ... https://www.journals.elsevier.com/thrombosis-research/most-cited-articles http://www.journals.elsevier.com/thrombosis-research ... of new information on thrombosis, hemostasis, and vascular biology to advance science and clinical care. The journal publishes ...
... may also occur after other surgeries. Hepatic artery thrombosis and primary non-function are the two ... Hepatic artery thrombosis may also be diagnosed using CT or MR imaging, which would show evidence of a blood clot within the ... Hepatic artery thrombosis occurs when a blood clot forms in the artery that provides blood flow to the liver. Hepatic artery ... Hepatic artery thrombosis can cause severe elevations in serum liver enzymes, AST and ALT. Often the AST is greater than the ...
Venous thrombosis associated with drainage from the brain (cerebral venous sinus thrombosis), eyes (retinal vein thrombosis), ... renal vein thrombosis), and ovaries (ovarian vein thrombosis) are more unusual forms of venous thrombosis and they are ... Deep vein thrombosis (DVT) is a type of venous thrombosis involving the formation of a blood clot in a deep vein, most commonly ... VTE, along with superficial vein thrombosis, are common types of venous thrombosis. DVT is classified as acute when the clots ...
... (RVT) is the formation of a clot in the vein that drains blood from the kidneys, ultimately leading to a ... "Renal Vein Thrombosis". Archived from the original on 31 March 2014. Retrieved 30 March 2014. "What is a Pulmonary Embolism". ... Asghar, M.; Ahmed, K.; Shah, S.S.; Siddique, M.K.; Dasgupta, P.; Khan, M.S. (August 2007). "Renal Vein Thrombosis". European ... From previous studies, it is known that long-distance air travel is associated with high risk of venous thrombosis. Long ...
... (SVT) is a blood clot formed in a superficial vein, a vein near the surface of the body. Usually ... SVT itself has limited significance (in terms of direct morbidity and mortality) when compared to a deep vein thrombosis (DVT ... deep vein thrombosis (DVT) was found in 24.6% of people with SVTs. However, because superficial veins lack muscular support, ...
... was opened in December 1988 as the Shenyang Research Institute of Thrombosis and Liaoning Province ... The Sujiatun Thrombosis Hospital, officially known as the Liaoning Provincial Thrombosis Treatment Center of Integrated Chinese ... It is a thrombosis treatment centre approved by the State Administration of Traditional Chinese Medicine, a class A Grade three ... published allegations by three individuals that thousands of Falun Gong practitioners had been killed at Sujiatun Thrombosis ...
... is known as hepatic vein thrombosis or Budd-Chiari syndrome. Portal vein thrombosis causes upper abdominal pain, possibly ... Portal vein thrombosis (PVT) is a vascular disease of the liver that occurs when a blood clot occurs in the hepatic portal vein ... If portal vein thrombosis develops due to pylephlebitis, signs of infection such as fever, chills, or night sweats may be ... The diagnosis of portal vein thrombosis is usually made with imaging confirming a clot in the portal vein; ultrasound is the ...
"Thrombosis and Haemostasis". www.thieme.com. "Thrombosis and Haemostasis". 2017 Journal Citation Reports. Web of Science ( ... Thrombosis and Haemostasis is a peer-review scientific journal of medicine. It is published by Thieme Medical Publishers. It is ... the official journal of several groups and societies: European Society of Cardiology (Thrombosis working group, Atherosclerosis ...
This is a rare disorder and can be of two types-septic cavernous thrombosis and aseptic cavernous thrombosis. The most common ... "Guidelines Cavernous sinus thrombosis" (PDF). "Cavernous sinus thrombosis - NHS Choices". www.nhs.uk. NHS Choices. Retrieved 27 ... Cavernous sinus thrombosis (CST) is the formation of a blood clot within the cavernous sinus, a cavity at the base of the brain ... Cavernous sinus thrombosis has a mortality rate of less than 20% in areas with access to antibiotics. Before antibiotics were ...
... (CVST), cerebral venous and sinus thrombosis or cerebral venous thrombosis (CVT), is the ... In cerebral venous thrombosis, blood clots usually form both in the veins of the brain and the venous sinuses. The thrombosis ... Disorders that cause, or increase the risk for systemic venous thrombosis are associated with central venous thromboses. In ... Wikimedia Commons has media related to Cerebral venous sinus thrombosis. "Intracranial venous thrombosis - Patient UK". UCH ...
... is a peer-reviewed medical review journal covering hematology, with a specific focus on ... "Seminars in Thrombosis and Hemostasis". 2018 Journal Citation Reports. Web of Science (Science ed.). Clarivate Analytics. 2019 ... disorders related to thrombosis and hemostasis. It was established in 1974 and is published eight times per year by Thieme ...
... (ATVB) is a peer-reviewed medical journal published on behalf of the ... From 1991 to 1994 it was published monthly under the title Arteriosclerosis and Thrombosis: A Journal of Vascular Biology (ISSN ... Clarivate Analytics, 2021). "About Arteriosclerosis, Thrombosis, and Vascular Biology". American Heart Association. Open Access ...
In a deep vein thrombosis (DVT), or in a superficial vein thrombosis where the thrombus is floating, an emergency situation ... Elliott, C. Gregory (2000). "The Diagnostic Approach to Deep Venous Thrombosis: Diagnostic Tests for Deep Vein Thrombosis". ... but of most importance is the detection of venous thrombosis. The most reliable sign of thrombosis (even when a good image and ... "Distribution of Thrombosis in Patients with Symptomatic Deep Vein Thrombosis: Implications for Simplifying the Diagnostic ...
The Journal of Thrombosis and Haemostasis is a monthly peer-reviewed medical journal covering research on thrombosis and ... "Journal of Thrombosis and Haemostasis". 2021 Journal Citation Reports. Web of Science (Science ed.). Clarivate Analytics. 2022 ... It is an official journal of the International Society on Thrombosis and Haemostasis. According to the Journal Citation Reports ...
This is a list of notable people who have died from coronary thrombosis, in chronological order. 1882: Charles Darwin (12 ... Deaths from coronary thrombosis, Lists of deaths from disease). ...
Journal of Thrombosis and Haemostasis, official medical journal of the ISTH Research and Practice in Thrombosis and Haemostasis ... such as thrombosis and hemophilia. It was founded in 1954 as the International Committee on Thrombosis and Haemostasis (ICTH). ... Research and Practice in Thrombosis and Haemostasis. The International Society on Thrombosis and Haemostasis (ISTH) advances ... The annual ISTH Congress is the premier event in the field of thrombosis and hemostasis featuring the latest scientific ...
Contraindications: Mammary tumors; estrogen-dependent tumors; history of cholestatic icterus; thrombophlebitis; thrombosis; ...
For the treatment of established deep vein thrombosis; central retinal and branch vein thrombosis; priapism; pulmonary ... and thrombosis. A small study compared to ancrod to heparin in preventing thrombosis when given to people undergoing arterial ... It is also indicated for the prevention of deep venous thrombosis after repair of the fractured neck of a femur. For the ... Geraghty AJ, Welch K (June 2011). "Antithrombotic agents for preventing thrombosis after infrainguinal arterial bypass surgery ...
Thrombosis and Haemostasis. 122 (3): a-1515-9630. doi:10.1055/A-1515-9630. PMID 34020488. Proietti, M; Romiti, GF; Olshansky, B ... Thrombosis and Vascular Biology; Council on Cardiovascular and Stroke Nursing; Council on Lifestyle and Cardiometabolic Health ... Thrombosis. 2013: 640723. doi:10.1155/2013/640723. PMC 3885278. PMID 24455237. Sanders, Gillian D.; Lowenstern, Angela; Borre, ... "Cardiac imaging for assessment of left atrial appendage stasis and thrombosis". Nature Reviews. Cardiology. 11 (8): 470-80. doi ...
Thrombosis. 2014: 714218. doi:10.1155/2014/714218. PMC 4293866. PMID 25610642. Hao, Z; Liu, M; Counsell, C; Wardlaw, JM; Lin, S ...
January 25 Adalberto Rosas López, polítician from (Ciudad Obregón), Sonora; thrombosis. Agustín Sauret (85), voice actor ("Ned ...
Thrombosis. 2014: 714218. doi:10.1155/2014/714218. PMC 4293866. PMID 25610642. Hao, Z; Liu, M; Counsell, C; Wardlaw, JM; Lin, S ...
"Rivaroxaban for the treatment of deep vein thrombosis and prevention of recurrent deep vein thrombosis and pulmonary embolism ... Specifically it is used to treat deep vein thrombosis and pulmonary emboli and prevent blood clots in atrial fibrillation and ... On July 1, 2011, the US Food and Drug Administration (FDA) approved rivaroxaban for prophylaxis of deep vein thrombosis (DVT), ... "FDA Approves Xarelto (rivaroxaban tablets) to Help Prevent Deep Vein Thrombosis in Patients Undergoing Knee or Hip Replacement ...
Deep vein thrombosis (DVT) prevention. DVTs may lead to pulmonary embolism (PE) in knee or hip replacement surgery patients. ... "U.S. FDA Approves Eliquis (apixaban) for the Treatment of Deep Vein Thrombosis (DVT) and Pulmonary Embolism (PE), and for the ... On 13 March 2014, it was approved for the additional indication of preventing deep vein thrombosis and pulmonary embolism in ... On 21 August 2014, the FDA approved apixaban for the additional indication of the treatment of recurring deep vein thrombosis ...
Deep vein thrombosis (DVT) occurs when a blood clot (thrombus) forms in one or more of the deep veins in the body, usually in ... Deep vein thrombosis can be serious because blood clots in the veins can break loose. The clots can then travel through the ... Lifestyle changes may help prevent deep vein thrombosis. Try these strategies:. * Move your legs. If youve had surgery or have ... The main causes of deep vein thrombosis (DVT) are damage to a vein from surgery or inflammation and damage due to infection or ...
Learn about the types of thrombosis conditions, where in the human body they happen, the various symptoms of each type, and ... Thrombosis is the medical term for a clot inside a blood vessel. ... Deep Vein Thrombosis News & Features * Deep Vein Thrombosis ... Stroke: "Diagnosis and Management of Cerebral Venous Thrombosis.". Johns Hopkins Medicine: "Cerebral Venous Sinus Thrombosis ( ... American College of Cardiology: "Upper Extremity Deep Vein Thrombosis.". Medscape: "Internal Jugular Vein Thrombosis," " ...
Factor V Leiden and Venous Thrombosis.  alert icon Archived: This Page Is No Longer Being Updated This web page is archived ... Factor V Leiden (FVL) and oral contraceptive (OC) use among women with venous thrombosis and controls* FVL†. Cases +. Controls ... Factor V Leiden (FVL) and oral contraceptive (OC) use among women with venous thrombosis and controls*. +. +. 25 ... Association between factor V Leiden (FVL) and oral contraceptive (OC) use in women with venous thrombosis. FVL*. +. 25 ...
Thrombosis of the venous channels in the brain is an uncommon cause of cerebral infarction relative to arterial disease, but it ... encoded search term (Cerebral Venous Thrombosis) and Cerebral Venous Thrombosis What to Read Next on Medscape ... Increased risk of cerebral venous sinus thrombosis with third- generation oral contraceptives. Cerebral Venous Sinus Thrombosis ... Cerebral venous thrombosis in adults. A study of 40 cases from Saudi Arabia. Stroke. 1995 Jul. 26(7):1193-5. [QxMD MEDLINE Link ...
Thrombosis of the venous channels in the brain is an uncommon cause of cerebral infarction relative to arterial disease, but it ... encoded search term (Cerebral Venous Thrombosis) and Cerebral Venous Thrombosis What to Read Next on Medscape ... Increased risk of cerebral venous sinus thrombosis with third- generation oral contraceptives. Cerebral Venous Sinus Thrombosis ... Cerebral Venous Thrombosis Differential Diagnoses. Updated: Oct 09, 2018 * Author: W Alvin McElveen, MD; Chief Editor: Helmi L ...
... on Factor VIII and Factor IX of the Scientific and Standardization Committee of the International Society on Thrombosis and ...
The great advantages that MRDTI has over other methods to detect thrombosis are that it is non-invasive, quick and reliable,? ... Radiologists in Nottingham have discovered a fast and accurate technique to diagnose deep vein thrombosis (DVT), which may be ... This technology potentially could help protect people at risk of a life-threatening venous thrombosis as well as reassuring ...
A multi-centre Canadian study has shown that blood thinners do not cure long-term consequences of Deep venous thrombosis (DVT ... Thrombosis Patients Do Not Benefit From Blood Thinners Personalised Printable Document (PDF). Please complete this form and ... A multi-centre Canadian study has shown that blood thinners do not cure long-term consequences of Deep venous thrombosis (DVT ... Thrombosis Patients Do Not Benefit From Blood Thinners. .article-author__avatar{float:left;}.article-author__avatar figure img{ ...
EndNote Styles - Open Atherosclerosis & Thrombosis Journal
Rutgers researchers describe a rare case of deep vein thrombosis in the arm of an otherwise healthy 85-year-old COVID patient. ...
Deep vein thrombosis (DVT) is a condition in which a blood clot develops in the deep veins, usually in the lower extremities. A ... Deep Vein Thrombosis & Pulmonary Embolism. CDC Yellow Book 2024. Travel by Air, Land & Sea ... The effect of flight-related behaviour on the risk of venous thrombosis after air travel. Br J Haematol. 2009;144(3):425-9. ... Prevention of VTE in nonsurgical patients: antithrombotic therapy and prevention of thrombosis, 9th edition: American College ...
If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Centers RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.. ...
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 ... Alan F. List, Donald C. Doll; Thrombosis Associated with Procainamide-Induced Lupus Anticoagulant. Acta Haematol 1 January 1989 ... One patient had a deep venous thrombosis and pulmonary embolism, while the other patient had a cerebrovascular accident. In ...
Deep vein thrombosis (DVT), is a blood clot that forms in a vein deep in the body, often in the leg. Learn about the causes, ... Deep vein thrombosis - discharge (Medical Encyclopedia) Also in Spanish * Deep venous thrombosis (Medical Encyclopedia) Also in ... Deep vein thrombosis, or DVT, is a blood clot that forms in a vein deep in the body. Most deep vein clots occur in the lower ... Deep Vein Thrombosis (American Academy of Orthopaedic Surgeons) * Venous Thromboembolism (Blood Clots) (Centers for Disease ...
... thrombosis of the dural sinus, cerebral veins, or bot ... Cerebral venous thrombosis and portal vein thrombosis: A ... Cortical vein thrombosis is thought to be even more rare than deep venous system thrombosis, occurring in only 116 patients in ... D, Coronal T1-weighted MRI sequence confirming thrombosis of the left vein of Labbé; the arrow indicates thrombosis of the ... OBJECTIVE Cerebral venous thrombosis (CVT), thrombosis of the dural sinus, cerebral veins, or both, is a rare cerebrovascular ...
Home » Instrumentation Laboratory wins 510(k) clearance for thrombosis assay. Instrumentation Laboratory wins 510(k) clearance ... which the company says can effectively rule out the possibility of thrombosis in patients. ... the test can be used to rule out in less than five minutes venous thromboembolism in patients suspected of deep vein thrombosis ...
Tag Archives: deep vein thrombosis. Deep Vein Thrombosis After Pleurectomy for Mesothelioma February 17, 2020. Alex Strauss ... Understanding DVT Deep vein thrombosis or DVT is when a blood clot forms in the deep veins of the arm, leg, or groin. If the ... The authors of a new study on deep vein thrombosis after pleurectomy say mesothelioma patients may be at special risk. They say ... Nearly 30 percent of the patients experienced deep vein thrombosis after pleurectomy. A third of those patients had no symptoms ...
The Royal Cork Yacht Club is based in Crosshaven, Cork, Ireland and is the worlds oldest yacht club founded in 1720. It is the organiser of the biennial Cork Week, widely regarded as Europes premier sailing event.. The club encompasses a wide variety of sailing activities from Optimist dinghies to racing National 18s and 1720s, Toppers, Lasers, RS Fevas and more ...read more. ...
Discover different methods to diagnose atrial fibrillation: Pulse check, electrocardiogram (ECG), echocardiograph. What factors increase the risk of AF?
Cortical vein thrombosis is a rare cause of stroke in children. Favorable prognosis relies on early detection, imaging, and ... Sebire G. Cerebral venous sinus thrombosis in children: risk factors, presentation, diagnosis and outcome. Brain. 2005;128(3): ... Parietal Lobe Infarction Secondary to Cortical Venous Thrombosis. .. Appl Radiol. 2022. ; 51. (. 6. ):. 9-11. . ... Parietal Lobe Infarction Secondary to Cortical Venous Thrombosis. Supplement to Applied Radiology. .. 2022. ;. 51. (. 6. ):. 9- ...
Autor desconhecido (‎2008)‎. IVIG : myocardial infarction, stroke and thrombosis. https://extranet.who.int/iris/restricted/ ...
Journal of Thrombosis and Thrombolysis. New Comprehensive Clinical Guidance in VTE New detailed consensus guidance from 58 ...
Among outpatients with suspected deep vein thrombosis in whom the clinical probability of venous thrombosis is judged to be low ... D-dimer strategy in thrombosis exclusion-a gold standard study in 100 patients suspected of deep venous thrombosis or pulmonary ... deep vein thrombosis unlikely) and those with a score of 2 to a higher probability group (deep vein thrombosis likely). In ... deep vein thrombosis likely and deep vein thrombosis unlikely.15 They specifically divided the moderate probability group (1 or ...
Deep vein thrombosis is caused by a blood clot that forms in one or more of the deep veins in your body, typically in your legs ... Deep Vein Thrombosis (DVT). Cleveland Clinic. July 18, 2019.. *Deep Vein Thrombosis (DVT): Symptoms and Causes. Mayo Clinic. ... Deep vein thrombosis (DVT) is caused by a blood clot that forms in one or more of the deep veins in your body, typically in ... Deep vein thrombosis can result from certain medical conditions that affect how your blood clots, according to the Mayo Clinic: ...
Clinical features that drive SARS-CoV-2 pathogenesis in humans include inflammation and thrombosis, but the mechanistic details ... Vascular Disease and Thrombosis in SARS-CoV-2-Infected Rhesus Macaques Cell. 2020 Nov 25;183(5):1354-1366.e13. doi: 10.1016/j. ... These results suggest a model in which critical interactions between inflammatory and thrombosis pathways lead to SARS-CoV-2- ... Clinical features that drive SARS-CoV-2 pathogenesis in humans include inflammation and thrombosis, but the mechanistic details ...
Other types of venous thrombosis, such as intra-abdominal and intracranial, are discussed in separate articles. ... ... Deep vein thrombosis (DVT) most commonly occurs in the lower limbs, however, are not uncommon in the upper limb and neck deep ... Deep vein thrombosis (DVT) most commonly occurs in the lower limbs, however, are not uncommon in the upper limb and neck deep ... Acute Venous Disease: Venous Thrombosis and Venous Trauma. J Vasc Surg. 2007;46(6):S25-S53. doi:10.1016/j.jvs.2007.08.037 ...
Comparison of Amlodipine vs Enalapril to Limit Occurrences of Thrombosis - CAMELOT. Nov 23, 2004 *. Print. ...
U.S. FDA Approves Eliquis (apixaban) for the Treatment of Deep Vein Thrombosis (DVT) and Pulmonary Embolism (PE), and for the ... ELIQUIS is indicated for the prophylaxis of deep vein thrombosis (DVT), which may lead to pulmonary embolism (PE), in patients ...
Johnson & Johnson/Janssen COVID-19 Vaccine and Thrombosis with Thrombocytopenia Syndrome (TTS): Update for Clinicians. ... This COCA Call will present the latest evidence on thrombosis with thrombocytopenia syndrome (TTS) after administration of the ... Johnson & Johnson/Janssen COVID-19 Vaccine and Cerebral Venous Sinus Thrombosis with Thrombocytopenia - Update for Clinicians ... Johnson & Johnson/Janssen COVID-19 Vaccine and Thrombosis with Thrombocytopenia Syndrome (TTS): Update for Clinicians ...
... in neonates include catheter thrombosis, occlusion or dislodgement and infection. Strategies to prevent catheter thrombosis and ... 42%; p = 0.002). There was no statistically significant differences in the risk of thrombosis (typical RR 0.93, 95% CI 0.58 to ... Continuous heparin infusion to prevent thrombosis and catheter occlusion in neonates with peripherally placed percutaneous ... Continuous heparin infusion to prevent thrombosis and catheter occlusion in neonates with peripherally placed percutaneous ...
  • The prevalence of activated protein C resistance was 20%-60% in selected groups of patients with venous thrombosis, depending on selection criteria. (cdc.gov)
  • conducted a case-control study to examine whether FVL might be a causative factor in venous thrombosis occurring as an uncommon but serious complication of oral contraceptive (OC) use. (cdc.gov)
  • Cases were women aged 15-49 years who experienced a first episode of venous thrombosis during 1988-1993 and who did not have cancer. (cdc.gov)
  • Do you agree that the relative risk of venous thrombosis in OC users was similar regardless of factor V genotype? (cdc.gov)
  • What evidence do these data provide for or against interaction between FVL and OC use in venous thrombosis? (cdc.gov)
  • Thrombosis of the venous channels in the brain is an uncommon cause of cerebral infarction relative to arterial disease, but it is an important consideration because of its potential morbidity. (medscape.com)
  • Knowledge of the anatomy of the venous system is essential in evaluating patients with cerebral venous thrombosis (CVT), since symptoms associated with the condition are related to the area of thrombosis. (medscape.com)
  • Cerebral hemorrhage also may be a presenting feature in patients with venous sinus thrombosis. (medscape.com)
  • Imaging procedures have led to easier recognition of venous sinus thrombosis (see the images below), offering the opportunity for early therapeutic measures. (medscape.com)
  • Many causative conditions have been described in cerebral venous thrombosis (CVT). (medscape.com)
  • Available at http://guideline.gov/content.aspx?id=47871&search=cerebral+venous+thrombosis . (medscape.com)
  • Schievink WI, Maya MM. Cerebral venous thrombosis in spontaneous intracranial hypotension. (medscape.com)
  • Cerebral venous sinus thrombosis as presenting feature of ulcerative colitis. (medscape.com)
  • Towbin A. The syndrome of latent cerebral venous thrombosis: its frequency and relation to age and congestive heart failure. (medscape.com)
  • Cerebral venous thrombosis in adults. (medscape.com)
  • Ameri A, Bousser MG. Cerebral venous thrombosis. (medscape.com)
  • Galarza M, Gazzeri R. Cerebral venous sinus thrombosis associated with oral contraceptives: the case for neurosurgery. (medscape.com)
  • Local thrombolytic therapy in deep cerebral venous thrombosis. (medscape.com)
  • Neurological and cognitive long-term outcome in patients with cerebral venous sinus thrombosis. (medscape.com)
  • Flores-Barragan JM, Hernandez-Gonzalez A, Gallardo-Alcaniz MJ, Del Real-Francia MA, Vaamonde-Gamo J. [Clinical and therapeutic heterogeneity of cerebral venous thrombosis: a description of a series of 20 cases. (medscape.com)
  • Wasay M, Kojan S, Dai AI, Bobustuc G, Sheikh Z. Headache in Cerebral Venous Thrombosis: incidence, pattern and location in 200 consecutive patients. (medscape.com)
  • D-dimer levels in patients with suspected acute cerebral venous thrombosis. (medscape.com)
  • Is measurement of D-dimer useful in the diagnosis of cerebral venous thrombosis? (medscape.com)
  • This technology potentially could help protect people at risk of a life-threatening venous thrombosis as well as reassuring those who are not in danger? (innovations-report.com)
  • A multi-centre Canadian study has shown that blood thinners do not cure long-term consequences of Deep venous thrombosis (DVT), the formation of blood clots in the lower limbs. (medindia.net)
  • Intracranial venous thrombosis. (bmj.com)
  • One patient had a deep venous thrombosis and pulmonary embolism, while the other patient had a cerebrovascular accident. (karger.com)
  • Unlike arterial strokes, cerebral venous thrombosis (CVT) has a wide spectrum of clinical presentations, tends to affect younger patients with a female predominance, and is often nonapoplectic in onset. (lww.com)
  • OBJECTIVE Cerebral venous thrombosis (CVT), thrombosis of the dural sinus, cerebral veins, or both, is a rare cerebrovascular disease. (lww.com)
  • The company says the test can be used to rule out in less than five minutes venous thromboembolism in patients suspected of deep vein thrombosis and pulmonary embolism. (massdevice.com)
  • 5 In older children, seizures are much less common and they will instead exhibit a triad of progressive, unremitting headache, altered mental status, and vomiting, especially in patients with venous sinus thrombosis. (appliedradiology.com)
  • Objective To summarise the evidence supporting the use of rapid D-dimer testing combined with estimation of clinical probability to exclude the diagnosis of deep venous thrombosis among outpatients. (bmj.com)
  • Results When the less sensitive SimpliRED D-dimer assay was used the three month incidence of venous thromboembolism was 0.5% (95% confidence interval 0.07% to 1.1%) among patients with a low clinical probability of deep vein thrombosis and normal D-dimer concentrations. (bmj.com)
  • When a highly sensitive D-dimer assay was used, the three month incidence of venous thromboembolism was 0.4% (0.04% to 1.1%) among outpatients with low or moderate clinical probability of deep vein thrombosis and a normal D-dimer concentration. (bmj.com)
  • Conclusions The combination of low clinical probability for deep vein thrombosis and a normal result from the SimpliRED D-dimer test safely excludes a diagnosis of acute venous thrombosis A normal result from a highly sensitive D-dimer test effectively rules out deep vein thrombosis among patients classified as having either low or moderate clinical probability of deep vein thrombosis. (bmj.com)
  • 4 Researchers into venous thrombosis now use this approach, combining D-dimer testing with estimation of the clinical probability of deep vein thrombosis. (bmj.com)
  • D-dimer concentrations are raised in the setting of acute deep vein thrombosis, 5 and normal concentrations are expected in the absence of acute venous thrombosis unless other, coexistent conditions that activate the coagulation system are present. (bmj.com)
  • Two clinical probability tools to estimate the probability of venous thrombosis are widely used. (bmj.com)
  • Other types of venous thrombosis, such as intra-abdominal and intracranial , are discussed in separate articles. (radiopaedia.org)
  • CDC recommends pausing the use of the J&J COVID-19 vaccine until the Advisory Committee on Immunization Practices is able to further review these cerebral venous sinus thrombosis cases in the context of thrombocytopenia and assess their potential significance. (cdc.gov)
  • Complications associated with peripherally placed percutaneous central venous catheters (PCVC) in neonates include catheter thrombosis, occlusion or dislodgement and infection. (cochrane.org)
  • Results: Deep vein thrombosis has showed an increased severity since the onset of covid with higher number of patients presenting with acute compartment syndrome requiring surgical intervention and with more number of cases showing extensive venous thrombosis. (who.int)
  • If you develop symptoms of a pulmonary embolism (PE) - a life-threatening complication of deep vein thrombosis - seek emergency medical help. (mayoclinic.org)
  • A deep vein thrombosis can break loose and cause a serious problem in the lung, called a pulmonary embolism . (medlineplus.gov)
  • The Centers for Disease Control and Prevention estimates that nearly 900,000 people each year will develop deep vein thrombosis (DVT) or. (medlineplus.gov)
  • Deep vein thrombosis (DVT) occurs when a blood clot (thrombus) forms in one or more of the deep veins in the body, usually in the legs. (mayoclinic.org)
  • Deep vein thrombosis can cause leg pain or swelling. (mayoclinic.org)
  • Deep vein thrombosis can be serious because blood clots in the veins can break loose. (mayoclinic.org)
  • Deep vein thrombosis can occur without noticeable symptoms. (mayoclinic.org)
  • This is called deep vein thrombosis (DVT). (mayoclinic.org)
  • The main causes of deep vein thrombosis (DVT) are damage to a vein from surgery or inflammation and damage due to infection or injury. (mayoclinic.org)
  • Many things can increase the risk of developing deep vein thrombosis (DVT). (mayoclinic.org)
  • Cancer, surgery, or using IV drugs can also cause jugular vein thrombosis. (webmd.com)
  • For example, cerebral infarction may occur with cortical vein or sagittal sinus thrombosis secondary to tissue congestion with obstruction. (medscape.com)
  • Long-Term Prognosis of Cerebral Vein and Dural Sinus Thrombosis. (medscape.com)
  • Radiologists in Nottingham have discovered a fast and accurate technique to diagnose deep vein thrombosis (DVT), which may be particularly helpful to pregnant women and travellers at risk of developing dangerous blood clots. (innovations-report.com)
  • Deep vein thrombosis (DVT) is a condition in which a blood clot develops in the deep veins, usually in the lower extremities. (cdc.gov)
  • Deep vein thrombosis, or DVT, is a blood clot that forms in a vein deep in the body. (medlineplus.gov)
  • The authors of a new study on deep vein thrombosis after pleurectomy say mesothelioma patients may be at special risk. (survivingmesothelioma.com)
  • Nearly 30 percent of the patients experienced deep vein thrombosis after pleurectomy. (survivingmesothelioma.com)
  • Understanding DVT Deep vein thrombosis or DVT is when a blood clot forms in the deep veins of the arm, leg, or groin. (survivingmesothelioma.com)
  • Left parietal lobe infarction secondary to cortical vein thrombosis (CVT) with hemorrhagic transformation. (appliedradiology.com)
  • The selected studies included more than 5000 patients and used a rapid D-dimer assay and explicit criteria to classify cases as having low, intermediate, or high clinical probability of deep vein thrombosis of the lower extremity among consecutive outpatients. (bmj.com)
  • Deep vein thrombosis is a common condition that often presents a diagnostic challenge to clinicians. (bmj.com)
  • Seventy five per cent of outpatients who present with signs and symptoms suggestive of deep vein thrombosis do not have the disease. (bmj.com)
  • One way to improve care and at the same time reduce the burden of ultrasound testing is to use a combination of two simple tests that, when combined, accurately exclude deep vein thrombosis. (bmj.com)
  • The first, developed by Wells et al, 2 12 uses a structured assessment of explicit historical and physical examination criteria (box) to stratify patients into low, moderate, and high risk of deep vein thrombosis. (bmj.com)
  • Deep vein thrombosis (DVT) is caused by a blood clot that forms in one or more of the deep veins in your body, typically in your legs. (everydayhealth.com)
  • Deep vein thrombosis (DVT) most commonly occurs in the lower limbs, however, are not uncommon in the upper limb and neck deep veins . (radiopaedia.org)
  • Other causes of coronary embolism include atrial fibrillation, left atrial tumours, bacterial endocarditis, atrial and ventricular mural thrombus, syphilis and pulmonary vein thrombosis [7]. (who.int)
  • We've compiled a list of symptoms, causes, and treatment for deep vein thrombosis and pulmonary embolisms with information from. (medlineplus.gov)
  • Aim : To study the severity and complication rates of deep vein thrombosis (DVT) during the covid pandemic as compared to a similar time frame before the pandemic. (who.int)
  • Materials and methods: A group of 80 patient diagnosed with deep vein thrombosis between April 2020 to November 2020 (Group A) were compared with a group of 80 patients diagnosed with deep vein thrombosis during the similar time frame in 2019 with respect to several parameters indicating the severity and complication rates of deep vein thrombosis. (who.int)
  • Extension into the jugular bulb may cause jugular foramen syndrome, while cranial nerve palsies may be seen in cavernous sinus thrombosis as a compressive phenomenon. (medscape.com)
  • Although coronary embolism due to mechanical valve thrombosis is encountered rarely, it is an important and serious complication. (who.int)
  • Mechanical valve thrombosis is a serious complication [2-4]. (who.int)
  • Do normal D-dimer levels reliably exclude cerebral sinus thrombosis? (medscape.com)
  • The entity implicated in the rare but potentially devastating cases of CVT and thrombocytopenia following adenovirus-based COVID-19 vaccine administration is now called vaccine-induced immune thrombotic thrombocytopenia (VITT), or thrombosis with thrombocytopenia syndrome. (lww.com)
  • This COCA Call will present the latest evidence on thrombosis with thrombocytopenia syndrome (TTS) after administration of the Johnson & Johnson/Janssen COVID-19 vaccine. (cdc.gov)
  • A predisposition to thrombosis in patients with procainamide-induced lupus anticoagulants is previously unrecognized. (karger.com)
  • We suggest that thrombosis may complicate treatment with procainamide in patients who develop the lupus anticoagulant. (karger.com)
  • Instrumentation Laboratory landed 510(k) clearance from the Food & Drug Administration for its HemosIL D-Dimer HS 500 assay, which the company says can effectively rule out the possibility of thrombosis in patients. (massdevice.com)
  • Lateral sinus thrombosis may be associated with headache and a pseudotumor cerebri-like picture. (medscape.com)
  • Left lateral sinus thrombosis demonstrated on magnetic resonance venography (MRV). (medscape.com)
  • Mas JL, Meder JF, Meary E, Bousser MG. Magnetic resonance imaging in lateral sinus hypoplasia and thrombosis. (medscape.com)
  • Canhão P, Batista P, Falcão F. Lumbar puncture and dural sinus thrombosis--a causal or casual association? (medscape.com)
  • Subarachnoid hemorrhage as the initial presentation of dural sinus thrombosis. (medscape.com)
  • Haemostasis and thrombosis : proceedings of the [First Florence Conference on Haemostasis and Thrombosis] / edited by G. G. Neri Serneri, C. R. M. Prentice. (who.int)
  • Aquaporin-1 regulates platelet procoagulant membrane dynamics and in vivo thrombosis. (bvsalud.org)
  • We hypothesized that water entry was mediated by the water channel aquaporin -1 (AQP1) and aimed to determine its role in the platelet procoagulant response and thrombosis . (bvsalud.org)
  • Ferro JM, Crassard I, Coutinho JM, Canhão P, Barinagarrementeria F, Cucchiara B. Decompressive surgery in cerebrovenous thrombosis: a multicenter registry and a systematic review of individual patient data. (medscape.com)
  • In this paper, we report a rare case of myocardial infarction, which occurred as a result of a coronary embolism in a patient with prosthetic mitral valve thrombosis. (who.int)
  • Mechanical valve thrombosis causes embolism rarely. (who.int)
  • In this study, we demonstrate endothelial disruption and vascular thrombosis in histopathologic sections of lungs from both humans and rhesus macaques infected with SARS-CoV-2. (nih.gov)
  • These results suggest a model in which critical interactions between inflammatory and thrombosis pathways lead to SARS-CoV-2-induced vascular disease. (nih.gov)
  • Clinical features that drive SARS-CoV-2 pathogenesis in humans include inflammation and thrombosis, but the mechanistic details underlying these processes remain to be determined. (nih.gov)
  • thrombosis of small blood vessels. (cdc.gov)
  • In several Swedish and Dutch populations, the prevalence of FVL was 2-7%, or about 10-fold higher than all previously identified genetic risk factors for thrombosis combined. (cdc.gov)
  • There was no statistically significant differences in the risk of thrombosis (typical RR 0.93, 95% CI 0.58 to 1.51), catheter related sepsis (typical RR 0.82, 95% CI 0.43 to 1.57), or extension of intraventricular haemorrhage (typical RR 0.50, 95% CI 0.19 to 1.28) between the two groups. (cochrane.org)
  • To assess the effectiveness of heparin for prevention of catheter related thrombosis. (cochrane.org)
  • Strategies to prevent catheter thrombosis and occlusion include the use of heparin. (cochrane.org)
  • Current OC use was defined as use within 30 days before the thrombosis event (cases) or index date (controls). (cdc.gov)
  • The Laboratory of Vascular Thrombosis and Inflammation, led by Dr. Yogen Kanthi, studies disease mechanism in venous thrombosis with a major area of focus on regulation of venous homeostasis. (nih.gov)
  • His team has studied the role of inlammasome activation and purine signaling in venous thrombosis (JCI, ATVB, Nature Communications). (nih.gov)
  • Our team studies disease mechanisms in venous thrombosis with a major area of focus on regulation of venous homeostasis. (nih.gov)
  • Our work utilizes human blood, tissues from patients with vascular disease, primary cultures endothelial cells, and mouse models of venous thrombosis. (nih.gov)
  • Available at http://guideline.gov/content.aspx?id=47871&search=cerebral+venous+thrombosis . (medscape.com)
  • Schievink WI, Maya MM. Cerebral venous thrombosis in spontaneous intracranial hypotension. (medscape.com)
  • Cerebral venous sinus thrombosis as presenting feature of ulcerative colitis. (medscape.com)
  • Towbin A. The syndrome of latent cerebral venous thrombosis: its frequency and relation to age and congestive heart failure. (medscape.com)
  • Cerebral venous thrombosis in adults. (medscape.com)
  • Ameri A, Bousser MG. Cerebral venous thrombosis. (medscape.com)
  • Galarza M, Gazzeri R. Cerebral venous sinus thrombosis associated with oral contraceptives: the case for neurosurgery. (medscape.com)
  • Local thrombolytic therapy in deep cerebral venous thrombosis. (medscape.com)
  • Neurological and cognitive long-term outcome in patients with cerebral venous sinus thrombosis. (medscape.com)
  • Flores-Barragan JM, Hernandez-Gonzalez A, Gallardo-Alcaniz MJ, Del Real-Francia MA, Vaamonde-Gamo J. [Clinical and therapeutic heterogeneity of cerebral venous thrombosis: a description of a series of 20 cases. (medscape.com)
  • Wasay M, Kojan S, Dai AI, Bobustuc G, Sheikh Z. Headache in Cerebral Venous Thrombosis: incidence, pattern and location in 200 consecutive patients. (medscape.com)
  • D-dimer levels in patients with suspected acute cerebral venous thrombosis. (medscape.com)
  • Is measurement of D-dimer useful in the diagnosis of cerebral venous thrombosis? (medscape.com)
  • CDC recommends pausing the use of the J&J COVID-19 vaccine until the Advisory Committee on Immunization Practices is able to further review these cerebral venous sinus thrombosis cases in the context of thrombocytopenia and assess their potential significance. (cdc.gov)
  • Do normal D-dimer levels reliably exclude cerebral sinus thrombosis? (medscape.com)
  • In addition to their well established role in hemostasis and thrombosis, it is now recognized that platelets play a pivotal role in orchestrating the process of inflammation. (nih.gov)
  • Thus platelets and clotting proteins which are essential in hemostasis/ thrombosis have indeed a dual role as initiators and modulators of the inflammatory process. (nih.gov)
  • Hemostasis and thrombosis / edited by E. J. Walter Bowie and A. A. Sharp. (who.int)
  • This statement was originally published as:Thrombolytic Therapy in Thrombosis. (nih.gov)
  • For making bibliographic reference to the statement in the electronic form displayed here, it is recommended that the following format be used: Thrombolytic Therapy in Thrombosis. (nih.gov)
  • A National Institutes of Health Consensus Development Conference, held at NIH April 10-12,1980, addressed the issue of thrombolytic therapy * for the management of acute deep-vein thrombosis and pulmonary embolism. (nih.gov)
  • A deep vein thrombosis can break loose and cause a serious problem in the lung, called a pulmonary embolism . (medlineplus.gov)
  • For over three decades, the primary method of therapy used by almost all physicians for the management of acute deep-vein thrombosis and pulmonary embolism has been anticoagulation. (nih.gov)
  • The reason that patients with acute deep-vein thrombosis and pulmonary embolism treated with anticoagulation alone are subject to these complications is that such therapy has no acute effect on previously formed thrombi or emboli. (nih.gov)
  • From these considerations it is apparent that ideal therapy for acute deep-vein thrombosis and pulmonary embolism requires either the surgical removal or lysis of the thrombus or embolus so as to restore to normal the hemodynamics and integrity of the vasculature, and the subsequent prevention of recurrence of thrombosis. (nih.gov)
  • See your doctor immediately if you have any signs or symptoms of deep vein thrombosis or pulmonary embolism (see the Wise Choices box). (nih.gov)
  • The Laboratory of Vascular Thrombosis and Inflammation (LVTI)has made seminal discoveries in COVID-19 pathology, being the first to identify neutrophil extracellular traps in patients with COVID-19 (JCI Insight), a new calprotectin biomarker for COVID-19 severity (J Leuk Biol), and the discovery of prothrombotic autoAntibodies in patients with COVID-19 (Science Translational Medicine). (nih.gov)
  • We leverage our strengths in inflammation and thrombosis , two processes at the heart of severe COVID-19 illness to understand this disease, and develop potential new treatments. (nih.gov)
  • The selectin family of receptors is now known to mediate the critical cell-cell interactions involved in leukocyte trafficking, thrombosis, and inflammation. (nih.gov)
  • These observations show that thrombosis and inflammation are biologically inseparable processes. (nih.gov)
  • The concentration of soluble CD40L in serum increases in acute coronary thrombosis and induces tissue factor expression on monocytes. (nih.gov)
  • Three factors predispose to thrombosis: injury to endothelium, alterations in normal blood flow, and alterations in blood hypercoagulability. (nih.gov)
  • We are interested in developing a deeper understanding of how innate immune circuits and communicate with coagulation and the vessel wall to license or restrict thrombosis. (nih.gov)
  • Human blood coagulation, haemostasis and thrombosis / edited by Rosemary Biggs and C. R. Rizza. (who.int)
  • Jugular vein thrombosis (JVT) was previously reported in MOE ( 5 ) and other conditions such as Lemierre syndrome, invasive fungal infection, or any inflammatory process including otitis media. (cdc.gov)
  • Deep vein thrombosis (DVT) is a condition in which a blood clot develops in the deep veins, usually in the lower extremities. (cdc.gov)
  • Deep vein thrombosis, or DVT, is a blood clot that forms in a vein deep in the body. (medlineplus.gov)
  • When a clot forms in a vein deep in the body, it's called deep vein thrombosis. (nih.gov)
  • Deep vein thrombosis has classic symptoms-for example swelling, pain, warmth, and redness on the leg," says Dr. Andrei Kindzelski, an NIH blood disease expert. (nih.gov)
  • Some people are more at risk for deep vein thrombosis than others. (nih.gov)
  • Usually people who develop deep vein thrombosis have some level of thrombophilia, which means their blood clots more rapidly or easily," Kindzelski says. (nih.gov)
  • But deep vein thrombosis can happen at any age. (nih.gov)
  • There are many ways to treat deep vein thrombosis. (nih.gov)
  • If you think you may be at risk for deep vein thrombosis, talk with your doctor. (nih.gov)
  • A local doctor diagnosed the problem immediately: deep vein thrombosis (DVT). (medlineplus.gov)
  • Mas JL, Meder JF, Meary E, Bousser MG. Magnetic resonance imaging in lateral sinus hypoplasia and thrombosis. (medscape.com)
  • Magnetic resonance imaging (MRI) with contrast media confirmed skull base osteomyelitis, evidenced by bone lysis and marrow enhancement of the clivus ( Figure , panels A-C). Both MRI and CT showed a right jugular vein thrombosis and cellulitis and abscess in the carotid and perivertebral spaces. (cdc.gov)
  • Haemostasis and thrombosis : proceedings of the [First Florence Conference on Haemostasis and Thrombosis] / edited by G. G. Neri Serneri, C. R. M. Prentice. (who.int)
  • A role for E-selectin in thrombosis has been suggested but not confirmed. (nih.gov)
  • Figure Legend: Figure 1 Ovary - Thrombosis in a female B6C3F1/N mouse from a chronic study. (nih.gov)