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.
Control of bleeding during or after surgery.
Control of bleeding performed through the channel of the endoscope. Techniques include use of lasers, heater probes, bipolar electrocoagulation, and local injection. Endoscopic hemostasis is commonly used to treat bleeding esophageal and gastrointestinal varices and ulcers.
Techniques for controlling bleeding.
Agents acting to arrest the flow of blood. Absorbable hemostatics arrest bleeding either by the formation of an artificial clot or by providing a mechanical matrix that facilitates clotting when applied directly to the bleeding surface. These agents function more at the capillary level and are not effective at stemming arterial or venous bleeding under any significant intravascular pressure.
Duration of blood flow after skin puncture. This test is used as a measure of capillary and platelet function.
The process of the interaction of BLOOD COAGULATION FACTORS that results in an insoluble FIBRIN clot.
Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation.
Formation and development of a thrombus or blood clot in the blood vessel.
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.
Bleeding or escape of blood from a vessel.
Pathological processes involving the integrity of blood circulation. Hemostasis depends on the integrity of BLOOD VESSELS, blood fluidity, and BLOOD COAGULATION. Majority of the hemostatic disorders are caused by disruption of the normal interaction between the VASCULAR ENDOTHELIUM, the plasma proteins (including BLOOD COAGULATION FACTORS), and PLATELETS.
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.
Use of a thrombelastograph, which provides a continuous graphic record of the physical shape of a clot during fibrin formation and subsequent lysis.
Endogenous substances, usually proteins, that are involved in the blood coagulation process.
Loss of blood during a surgical procedure.
A cellulose of varied carboxyl content retaining the fibrous structure. It is commonly used as a local hemostatic and as a matrix for normal blood coagulation.
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.
Incision of tissues for injection of medication or for other diagnostic or therapeutic procedures. Punctures of the skin, for example may be used for diagnostic drainage; of blood vessels for diagnostic imaging procedures.
Bleeding from a PEPTIC ULCER that can be located in any segment of the GASTROINTESTINAL TRACT.
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.
Hemorrhage following any surgical procedure. It may be immediate or delayed and is not restricted to the surgical wound.
Spontaneous or near spontaneous bleeding caused by a defect in clotting mechanisms (BLOOD COAGULATION DISORDERS) or another abnormality causing a structural flaw in the blood vessels (HEMOSTATIC DISORDERS).
An autologous or commercial tissue adhesive containing FIBRINOGEN and THROMBIN. The commercial product is a two component system from human plasma that contains more than fibrinogen and thrombin. The first component contains highly concentrated fibrinogen, FACTOR VIII, fibronectin, and traces of other plasma proteins. The second component contains thrombin, calcium chloride, and antifibrinolytic agents such as APROTININ. Mixing of the two components promotes BLOOD CLOTTING and the formation and cross-linking of fibrin. The tissue adhesive is used for tissue sealing, HEMOSTASIS, and WOUND HEALING.
Bleeding in any segment of the GASTROINTESTINAL TRACT from ESOPHAGUS to RECTUM.
An enzyme formed from PROTHROMBIN that converts FIBRINOGEN to FIBRIN.
Procedures using an electrically heated wire or scalpel to treat hemorrhage (e.g., bleeding ulcers) and to ablate tumors, mucosal lesions, and refractory arrhythmias. It is different from ELECTROSURGERY which is used more for cutting tissue than destroying and in which the patient is part of the electric circuit.
The natural enzymatic dissolution of FIBRIN.
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.
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.
Agents that cause clotting.
The process whereby PLATELETS adhere to something other than platelets, e.g., COLLAGEN; BASEMENT MEMBRANE; MICROFIBRILS; or other "foreign" surfaces.
Laboratory tests for evaluating the individual's clotting mechanism.
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.
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.
Sterile, gelatin-base surgical sponge applied topically as an adjunct to hemostasis when the control of bleeding by conventional procedures is ineffective to reduce capillary ooze or is impractical. (From AMA Drug Evaluations Annual, 1994, p797)
Activated form of factor VII. Factor VIIa activates factor X in the extrinsic pathway of blood coagulation.
Hand-held tools or implements used by health professionals for the performance of surgical tasks.
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.
The classic hemophilia resulting from a deficiency of factor VIII. It is an inherited disorder of blood coagulation characterized by a permanent tendency to hemorrhage.
Blood-coagulation factor VIII. Antihemophilic factor that is part of the factor VIII/von Willebrand factor complex. Factor VIII is produced in the liver and acts in the intrinsic pathway of blood coagulation. It serves as a cofactor in factor X activation and this action is markedly enhanced by small amounts of thrombin.
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.
The number of PLATELETS per unit volume in a sample of venous BLOOD.
Substances used to cause adherence of tissue to tissue or tissue to non-tissue surfaces, as for prostheses.
Heat- and storage-stable plasma protein that is activated by tissue thromboplastin to form factor VIIa in the extrinsic pathway of blood coagulation. The activated form then catalyzes the activation of factor X to factor Xa.
Retraction of a clot resulting from contraction of PLATELET pseudopods attached to FIBRIN strands. The retraction is dependent on the contractile protein thrombosthenin. Clot retraction is used as a measure of platelet function.
A protein derived from FIBRINOGEN in the presence of THROMBIN, which forms part of the blood clot.
The main artery of the thigh, a continuation of the external iliac artery.
An endogenous family of proteins belonging to the serpin superfamily that neutralizes the action of thrombin. Six naturally occurring antithrombins have been identified and are designated by Roman numerals I to VI. Of these, Antithrombin I (see FIBRIN) and ANTITHROMBIN III appear to be of major importance.
Group of hemorrhagic disorders in which the VON WILLEBRAND FACTOR is either quantitatively or qualitatively abnormal. They are usually inherited as an autosomal dominant trait though rare kindreds are autosomal recessive. Symptoms vary depending on severity and disease type but may include prolonged bleeding time, deficiency of factor VIII, and impaired platelet adhesion.
Methods to repair breaks in tissue caused by trauma or to close surgical incisions.
A subspecialty of internal medicine concerned with morphology, physiology, and pathology of the blood and blood-forming tissues.
A disorder characterized by procoagulant substances entering the general circulation causing a systemic thrombotic process. The activation of the clotting mechanism may arise from any of a number of disorders. A majority of the patients manifest skin lesions, sometimes leading to PURPURA FULMINANS.
A 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.
Agents that prevent clotting.
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.
Surface glycoproteins on platelets which have a key role in hemostasis and thrombosis such as platelet adhesion and aggregation. Many of these are receptors.
A dry artificial sterile sponge of fibrin prepared by clotting with thrombin a foam or solution of fibrinogen. It is used in conjunction with thrombin as a hemostatic in surgery at sites where bleeding cannot be controlled by more common methods. (From Martindale, The Extra Pharmacopoeia, 30th ed, p648)
Platelet membrane glycoprotein complex essential for normal platelet adhesion and clot formation at sites of vascular injury. It is composed of three polypeptides, GPIb alpha, GPIb beta, and GPIX. Glycoprotein Ib functions as a receptor for von Willebrand factor and for thrombin. Congenital deficiency of the GPIb-IX complex results in Bernard-Soulier syndrome. The platelet glycoprotein GPV associates with GPIb-IX and is also absent in Bernard-Soulier syndrome.
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.
A tissue adhesive that is applied as a monomer to moist tissue and polymerizes to form a bond. It is slowly biodegradable and used in all kinds of surgery, including dental.
A hereditary deficiency of blood coagulation factor XI (also known as plasma thromboplastin antecedent or PTA or antihemophilic factor C) resulting in a systemic blood-clotting defect called hemophilia C or Rosenthal's syndrome, that may resemble classical hemophilia.
Hemorrhagic and thrombotic disorders resulting from abnormalities or deficiencies of coagulation proteins.
Techniques for securing together the edges of a wound, with loops of thread or similar materials (SUTURES).
Material, usually gauze or absorbent cotton, used to cover and protect wounds, to seal them from contact with air or bacteria. (From Dorland, 27th ed)
A collection of blood outside the BLOOD VESSELS. Hematoma can be localized in an organ, space, or tissue.
Plugs or cylinders made of cotton, sponge, or other absorbent material. They are used in surgery to absorb fluids such as blood or drainage.
Endoscopic examination, therapy or surgery of the gastrointestinal tract.
Laboratory examination used to monitor and evaluate platelet function in a patient's blood.
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.
Very large BONE MARROW CELLS which release mature BLOOD PLATELETS.
Stable blood coagulation factor involved in the intrinsic pathway. The activated form XIa activates factor IX to IXa. Deficiency of factor XI is often called hemophilia C.
Platelet membrane glycoprotein IIb is an integrin alpha subunit that heterodimerizes with INTEGRIN BETA3 to form PLATELET GLYCOPROTEIN GPIIB-IIIA COMPLEX. It is synthesized as a single polypeptide chain which is then postranslationally cleaved and processed into two disulfide-linked subunits of approximately 18 and 110 kDa in size.
Two small peptide chains removed from the N-terminal segment of the alpha chains of fibrinogen by the action of thrombin during the blood coagulation process. Each peptide chain contains 18 amino acid residues. In vivo, fibrinopeptide A is used as a marker to determine the rate of conversion of fibrinogen to fibrin by thrombin.
A group of compounds having the general formula CH2=C(CN)-COOR; it polymerizes on contact with moisture; used as tissue adhesive; higher homologs have hemostatic and antibacterial properties.
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.
A class of receptors that are activated by the action of PROTEINASES. The most notable examples are the THROMBIN RECEPTORS. The receptors contain cryptic ligands that are exposed upon the selective proteolysis of specific N-terminal cleavage sites.
A deficiency of blood coagulation factor IX inherited as an X-linked disorder. (Also known as Christmas Disease, after the first patient studied in detail, not the holy day.) Historical and clinical features resemble those in classic hemophilia (HEMOPHILIA A), but patients present with fewer symptoms. Severity of bleeding is usually similar in members of a single family. Many patients are asymptomatic until the hemostatic system is stressed by surgery or trauma. Treatment is similar to that for hemophilia A. (From Cecil Textbook of Medicine, 19th ed, p1008)
Not an aneurysm but a well-defined collection of blood and CONNECTIVE TISSUE outside the wall of a blood vessel or the heart. It is the containment of a ruptured blood vessel or heart, such as sealing a rupture of the left ventricle. False aneurysm is formed by organized THROMBUS and HEMATOMA in surrounding tissue.
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.
The transfer of blood platelets from a donor to a recipient or reinfusion to the donor.
A synthetic analog of the pituitary hormone, ARGININE VASOPRESSIN. Its action is mediated by the VASOPRESSIN receptor V2. It has prolonged antidiuretic activity, but little pressor effects. It also modulates levels of circulating FACTOR VIII and VON WILLEBRAND FACTOR.
Stable blood coagulation factor activated by contact with the subendothelial surface of an injured vessel. Along with prekallikrein, it serves as the contact factor that initiates the intrinsic pathway of blood coagulation. Kallikrein activates factor XII to XIIa. Deficiency of factor XII, also called the Hageman trait, leads to increased incidence of thromboembolic disease. Mutations in the gene for factor XII that appear to increase factor XII amidolytic activity are associated with HEREDITARY ANGIOEDEMA TYPE III.
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.
Rod-shaped storage granules for VON WILLEBRAND FACTOR specific to endothelial cells.
Drugs or agents which antagonize or impair any mechanism leading to blood platelet aggregation, whether during the phases of activation and shape change or following the dense-granule release reaction and stimulation of the prostaglandin-thromboxane system.
The vitamin K-dependent cofactor of activated PROTEIN C. Together with protein C, it inhibits the action of factors VIIIa and Va. A deficiency in protein S; (PROTEIN S DEFICIENCY); can lead to recurrent venous and arterial thrombosis.
Endogenous 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.
A subnormal level of BLOOD PLATELETS.
Starches that have been chemically modified so that a percentage of OH groups are substituted with 2-hydroxyethyl ether groups.
A member of the serpin superfamily found in plasma that inhibits the lysis of fibrin clots which are induced by plasminogen activator. It is a glycoprotein, molecular weight approximately 70,000 that migrates in the alpha 2 region in immunoelectrophoresis. It is the principal plasmin inactivator in blood, rapidly forming a very stable complex with plasmin.
Procedure to accelerate the ability of a patient to walk or move about by reducing the time to AMBULATION. It is characterized by a shorter period of hospitalization or recumbency than is normally practiced.
Elements of limited time intervals, contributing to particular results or situations.
Procedures of applying ENDOSCOPES for disease diagnosis and treatment. Endoscopy involves passing an optical instrument through a small incision in the skin i.e., percutaneous; or through a natural orifice and along natural body pathways such as the digestive tract; and/or through an incision in the wall of a tubular structure or organ, i.e. transluminal, to examine or perform surgery on the interior parts of the body.
Storage-stable blood coagulation factor acting in the intrinsic pathway. Its activated form, IXa, forms a complex with factor VIII and calcium on platelet factor 3 to activate factor X to Xa. Deficiency of factor IX results in HEMOPHILIA B (Christmas Disease).
A type of stress exerted uniformly in all directions. Its measure is the force exerted per unit area. (McGraw-Hill Dictionary of Scientific and Technical Terms, 6th ed)
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.
Reduction of blood viscosity usually by the addition of cell free solutions. Used clinically (1) in states of impaired microcirculation, (2) for replacement of intraoperative blood loss without homologous blood transfusion, and (3) in cardiopulmonary bypass and hypothermia.
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.
Disorders caused by abnormalities in platelet count or function.
Obstruction of a blood vessel (embolism) by a blood clot (THROMBUS) in the blood stream.
A member of the serpin family of proteins. It inhibits both the tissue-type and urokinase-type plasminogen activators.
Endoscopic examination, therapy or surgery of the interior of the stomach.
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.
Division of tissues by a high-frequency current applied locally with a metal instrument or needle. (Stedman, 25th ed)
A polypeptide substance comprising about one third of the total protein in mammalian organisms. It is the main constituent of SKIN; CONNECTIVE TISSUE; and the organic substance of bones (BONE AND BONES) and teeth (TOOTH).
The introduction of whole blood or blood component directly into the blood stream. (Dorland, 27th ed)
Methods of creating machines and devices.
Adenosine 5'-(trihydrogen diphosphate). An adenine nucleotide containing two phosphate groups esterified to the sugar moiety at the 5'-position.
Agents that prevent fibrinolysis or lysis of a blood clot or thrombus. Several endogenous antiplasmins are known. The drugs are used to control massive hemorrhage and in other coagulation disorders.
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.
The active sympathomimetic hormone from the ADRENAL MEDULLA. It stimulates both the alpha- and beta- adrenergic systems, causes systemic VASOCONSTRICTION and gastrointestinal relaxation, stimulates the HEART, and dilates BRONCHI and cerebral vessels. It is used in ASTHMA and CARDIAC FAILURE and to delay absorption of local ANESTHETICS.
A product formed from skin, white connective tissue, or bone COLLAGEN. It is used as a protein food adjuvant, plasma substitute, hemostatic, suspending agent in pharmaceutical preparations, and in the manufacturing of capsules and suppositories.
A method of hemostasis utilizing various agents such as Gelfoam, silastic, metal, glass, or plastic pellets, autologous clot, fat, and muscle as emboli. It has been used in the treatment of spinal cord and INTRACRANIAL ARTERIOVENOUS MALFORMATIONS, renal arteriovenous fistulas, gastrointestinal bleeding, epistaxis, hypersplenism, certain highly vascular tumors, traumatic rupture of blood vessels, and control of operative hemorrhage.
The process of generating thrombocytes (BLOOD PLATELETS) from the pluripotent HEMATOPOIETIC STEM CELLS in the BONE MARROW via the MEGAKARYOCYTES. The humoral factor with thrombopoiesis-stimulating activity is designated THROMBOPOIETIN.
A fibrin-stabilizing plasma enzyme (TRANSGLUTAMINASES) that is activated by THROMBIN and CALCIUM to form FACTOR XIIIA. It is important for stabilizing the formation of the fibrin polymer (clot) which culminates the coagulation cascade.
An integrin alpha subunit that primarily combines with INTEGRIN BETA1 to form the INTEGRIN ALPHA2BETA1 heterodimer. It contains a domain which has homology to collagen-binding domains found in von Willebrand factor.
Dilated blood vessels in the ESOPHAGUS or GASTRIC FUNDUS that shunt blood from the portal circulation (PORTAL SYSTEM) to the systemic venous circulation. Often they are observed in individuals with portal hypertension (HYPERTENSION, PORTAL).
Nonexpendable apparatus used during surgical procedures. They are differentiated from SURGICAL INSTRUMENTS, usually hand-held and used in the immediate operative field.
A family of proteinase-activated receptors that are specific for THROMBIN. They are found primarily on PLATELETS and on ENDOTHELIAL CELLS. Activation of thrombin receptors occurs through the proteolytic action of THROMBIN, which cleaves the N-terminal peptide from the receptor to reveal a new N-terminal peptide that is a cryptic ligand for the receptor. The receptors signal through HETEROTRIMERIC GTP-BINDING PROTEINS. Small synthetic peptides that contain the unmasked N-terminal peptide sequence can also activate the receptor in the absence of proteolytic activity.
Treatment of varicose veins, hemorrhoids, gastric and esophageal varices, and peptic ulcer hemorrhage by injection or infusion of chemical agents which cause localized thrombosis and eventual fibrosis and obliteration of the vessels.
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.
Lasers in which a gas lasing medium is stimulated to emit light by an electric current or high-frequency oscillator.
Bleeding from blood vessels in the UTERUS, sometimes manifested as vaginal bleeding.

Primary haemostasis: sticky fingers cement the relationship. (1/1215)

Platelet aggregation to form a haemostatic plug, or thrombus, plays a key role in preventing bleeding from a wound. Recent studies have provided new insights into how platelet receptors are deployed during the interactions with the vascular subendothelial matrix that lead to haemostatic plug formation.  (+info)

Socioeconomic status and determinants of hemostatic function in healthy women. (2/1215)

Hemostatic factors are reported to be associated with coronary heart disease (CHD). Socioeconomic status (SES) is 1 of the determinants of the hemostatic profile, but the factors underlying this association are not well known. Our aim was to examine determinants of the socioeconomic differences in hemostatic profile. Between 1991 and 1994, we studied 300 healthy women, aged 30 to 65 years, who were representative of women living in the greater Stockholm area. Fibrinogen, factor VII mass concentration (FVII:Ag), activated factor VII (FVIIa), von Willebrand factor (vWF), and plasminogen activator inhibitor-1 (PAI-1) were measured. Educational attainment was used as a measure of SES. Low educational level and an unfavorable hemostatic profile were both associated with older age, unhealthful life style, psychosocial stress, atherogenic biochemical factors, and hypertension. Levels of hemostatic factors increased with lower educational attainment. Independently of age, the differences between the lowest (mandatory) and highest (college/university) education in FVII:Ag levels were 41 microg/L (95% confidence interval [CI], 15 to 66 microg/L, P=0.001), 0.26 g/L (95% CI, 0.10 to 0.42 g/L, P=0.001) in fibrinogen levels, and 0.11 U/mL (95% CI, 0.09 to 0.12 U/mL, P=0.03) in levels of vWF. The corresponding differences in FVIIa and PAI-1 were not statistically significant. With further adjustment for menopausal status, family history of CHD, marital status, psychosocial stress, lifestyle patterns, biochemical factors, and hypertension, statistically significant differences between mandatory and college/university education were observed in FVII:Ag (difference=34 microg/L; 95% CI, 2 to 65 microg/L, P=0.05) but not in fibrinogen (difference=0.03 g/L; 95% CI, -0.13 to 0.19 g/L, P=0.92) or in vWF (difference=0.06 U/mL; 95% CI, -0.10 to 0.22 U/mL, P=0.45). An educational gradient was most consistent and statistically significant for FVII:Ag, fibrinogen, and vWF. Age, psychosocial stress, unhealthful life style, atherogenic biochemical factors, and hypertension mediated the association of low educational level with elevated levels of fibrinogen and vWF. Psychosocial stress and unhealthful life style were the most important contributing factors. There was an independent association between education and FVII:Ag, which could not be explained by any of these factors.  (+info)

Alpha2-antiplasmin gene deficiency in mice is associated with enhanced fibrinolytic potential without overt bleeding. (3/1215)

alpha2-antiplasmin (alpha2-AP) is the main physiologic plasmin inhibitor in mammalian plasma. Inactivation of the murine alpha2-AP gene was achieved by replacing, through homologous recombination in embryonic stem cells, a 7-kb genomic sequence encoding the entire murine protein (exon 2 through part of exon 10, including the stop codon) with the neomycin resistance expression cassette. Germline transmission of the mutated allele was confirmed by Southern blot analysis. Mendelian inheritance of the inactivated alpha2-AP allele was observed, and homozygous deficient (alpha2-AP-/-) mice displayed normal fertility, viability, and development. Reverse transcription-polymerase chain reaction confirmed the absence of alpha2-AP mRNA in kidney and liver from alpha2-AP-/- mice, in contrast to wild-type (alpha2-AP+/+) mice. Immunologic and functional alpha2-AP levels were undetectable in plasma of alpha2-AP-/- mice, and were about half of wild-type in heterozygous littermates (alpha2-AP+/-). Other hemostasis parameters, including plasminogen activator inhibitor-1, plasminogen, fibrinogen, hemoglobin, hematocrit, and blood cell counts were comparable for alpha2-AP+/+, alpha2-AP+/-, and alpha2-AP-/- mice. After amputation of tail or toe tips, bleeding stopped spontaneously in alpha2-AP+/+, as well as in alpha2-AP+/- and alpha2-AP-/- mice. Spontaneous lysis after 4 hours of intravenously injected 125I-fibrin-labeled plasma clots was significantly higher in alpha2-AP-/- than in alpha2-AP+/+ mice when injecting clots prepared from alpha2-AP+/+ plasma (78% +/- 5% v 46% +/- 9%; mean +/- SEM, n = 6 to 7; P =.02) or from alpha2-AP-/- plasma (81% +/- 5% v 46% +/- 5%; mean +/- SEM, n = 5; P =.008). Four to 8 hours after endotoxin injection, fibrin deposition in the kidneys was significantly reduced in alpha2-AP-/- mice, as compared with alpha2-AP+/+ mice (P +info)

Thrombelastographic changes and early rebleeding in cirrhotic patients with variceal bleeding. (4/1215)

BACKGROUND: Routine coagulation tests do not necessarily reflect haemostasis in vivo in cirrhotic patients, particularly those who have bleeding varices. Thrombelastography (TEG) can provide a global assessment of haemostatic function from initial clot formation to clot dissolution. AIM: To evaluate TEG changes in cirrhotic patients with variceal bleeding and their association with early rebleeding. PATIENTS/METHODS: Twenty cirrhotic patients with active variceal bleeding had serial TEG and routine coagulation tests daily for seven days. The TEG variables before the day of rebleeding (n = 6) were compared with those of patients without rebleeding (n = 14). RESULTS: Baseline characteristics of the rebleeding and non-rebleeding groups were comparable apart from a higher incidence of uncontrolled infection on the day of rebleeding in the rebleeding group (p = 0.007). The patients in the rebleeding group were more hypocoagulable before the day of rebleeding as shown by longer r (42 v 24 mm, p < 0.001) and k (48 v 13 mm, p < 0.001) and smaller a (12 v 38 degrees, p < 0.001) compared with the mean of daily results of the non-rebleeding group. Routine coagulation tests, however, showed no significant differences between the two groups. CONCLUSION: The results of serial TEG measurements suggest that hypocoagulability may be associated with early rebleeding in cirrhotic patients.  (+info)

Pravastatin therapy in hyperlipidemia: effects on thrombus formation and the systemic hemostatic profile. (5/1215)

OBJECTIVES: The study sought to determine the effects of lipid-lowering with pravastatin on the systemic fibrinolytic profile and on thrombus formation under dynamic flow conditions. BACKGROUND: Lowering cholesterol (C) decreases clinical events in coronary artery disease (CAD) patients, but an analysis of the effects of lipid-lowering on the entire hemostatic and thrombotic profile has not been conducted. METHODS: We prospectively studied 93 stable patients with untreated low-density lipoprotein cholesterol (LDL-C) >145 mg/dl. The CAD patients received pravastatin, and non-CAD patients were randomized to pravastatin versus placebo (double-blind). Thrombus formation upon an injured vascular surface was assessed in a substudy of 40 patients with a previously validated ex vivo perfusion chamber system. Systemic hemostatic markers and thrombus formation were evaluated at baseline, three and six months. RESULTS: Placebo produced no changes in either the lipid profile, any of the hemostatic markers, or the ex vivo thrombus formation. Both pravastatin groups (CAD and non-CAD) showed decreased LDL-C by 30% within 6 weeks (188 to 126 mg/dl, p < 0.001 vs. baseline), and decreased plasminogen activator inhibitor-1 at 3- and 6-month follow-up compared to baseline (15% to 18% decrease at 3 months and 21% to 23% at 6 months). For the tissue plasminogen activator antigen, CAD and non-CAD groups showed significant decreases at 6 months compared to baseline (10% and 13%, respectively). No significant changes were observed with treatment in d-dimer, fibrinopeptide A, prothrombin fragment F1.2, factor VIIa, von Willebrand factor, or C-reactive protein. Fibrinogen levels were significantly increased at 6 months compared to baseline, though still below the upper normal limit. In the perfusion chamber substudy, there was a decrease in thrombus area in non-CAD patients treated with pravastatin at both 3 and 6 months compared to baseline (by 21% and 34%, respectively). The CAD patients showed decreases in thrombus formation by 13% at 3 months, and by 16% at 6 months. The change in LDL-C- correlated modestly with the change in thrombus formation (r = 0.49; p < 0.01). CONCLUSIONS: Pravastatin therapy significantly decreased thrombus formation and improved the fibrinolytic profile in patients with and without CAD. These early effects may, in part, explain the benefit rendered in primary and secondary prevention of CAD.  (+info)

Neutrophil activation and hemostatic changes in healthy donors receiving granulocyte colony-stimulating factor. (6/1215)

Granulocyte colony-stimulating factor (G-CSF) enhances neutrophil functions in vitro and in vivo. It is known that neutrophil-derived products can alter the hemostatic balance. To understand whether polymorphonuclear leukocyte (PMN) activation, measured as PMN degranulation and phenotypical change, may be associated to hemostatic alterations in vivo, we have studied the effect of recombinant human G-CSF (rHuG-CSF) administration on leukocyte parameters and hemostatic variables in healthy donors of hematopoietic progenitor cells (HPCs). Twenty-six consecutive healthy donors receiving 10 micrograms/kg/d rHuG-CSF subcutaneously for 5 to 7 days to mobilize HPCs for allogeneic transplants were included in the study. All of them responded to rHuG-CSF with a significant white blood cell count increase. Blood samples were drawn before therapy on days 2 and 5 and 1 week after stopping rHuG-CSF treatment. The following parameters were evaluated: (1) PMN activation parameters, ie, surface CD11b/CD18 antigen expression, plasma elastase antigen levels and cellular elastase activity; (2) plasma markers of endothelium activation, ie, thrombomodulin (TM) and von Willebrand factor (vWF) antigens; (3) plasma markers of blood coagulation activation, ie, F1+2, TAT complex, D-dimer; and (4) mononuclear cell (MNC) procoagulant activity (PCA) expression. The results show that, after starting rHuG-CSF, an in vivo PMN activation occurred, as demonstrated by the significant increment of surface CD11b/CD18 and plasma elastase antigen levels. Moreover, PMN cellular elastase activity, which was significantly increased at 1 day of treatment, returned to baseline at day 5 to 6, in correspondence with the elastase antigen peak in the circulation. This change was accompanied by a parallel significant increase in plasma levels of the two endothelial and the three coagulation markers. The PCA generated in vitro by unstimulated MNC isolated from rHuG-CSF-treated subjects was not different from that of control cells from untreated subjects. However, endotoxin-stimulated MNC isolated from on-treatment individuals produced significantly more PCA compared with both baseline and control samples. All of the parameters were decreased or normal 1 week after stopping treatment. These data show that rHuG-CSF induces PMN activation and transiently affects some hemostatic variables in healthy HPC donor subjects. The clinical significance of these findings remains to be established.  (+info)

Hormone replacement therapy, inflammation, and hemostasis in elderly women. (7/1215)

Lipid-lowering by postmenopausal hormone therapy (HRT) explains only partly the assumed coronary risk reduction associated with therapy. To explore other possible mechanisms, we studied associations of HRT use with inflammation and hemostasis risk markers in women >/=65 years of age. Subjects were selected from 3393 participants in the fourth year examination of the Cardiovascular Health Study, an observational study of vascular disease risk factors. After excluding women with vascular disease, we compared levels of inflammation and hemostasis variables in the 230 women using unopposed estrogen and 60 using estrogen/progestin, with those of 196 nonusers selected as controls. Compared with nonusers, unopposed estrogen use was associated with 59% higher mean C-reactive protein (P<0.001), but with modestly lower levels of other inflammation indicators, fibrinogen, and alpha-1 acid glycoprotein (P<0.001). Factor VIIc was 16% higher among estrogen users (P<0.001), but this was not associated with higher thrombin production (prothrombin fragment 1-2), or increased fibrin breakdown (D-dimer). Concentration of plasminogen activator inhibitor-1 was 50% lower in both using groups (P<0.001) compared with nonusers, and this was associated with higher plasmin-antiplasmin complex: 8% higher in estrogen and 18% higher in estrogen/progestin users (P<0. 05). Relationships between the markers and hormone use were less pronounced in estrogen/progestin users, with no association for C-reactive protein except in women in upper 2 tertiles of body mass index (P for interaction, 0.02). The direction and strength of the associations of HRT use with inflammation markers differed depending on the protein, so it is not clear whether HRT confers coronary risk reduction through an inflammation-sensitive mechanism. Associations with hemostasis markers indicated no association with evidence of procoagulation and a possible association with increased fibrinolytic activity.  (+info)

Strategy for balancing anticoagulation and hemostasis in aortocoronary bypass surgery: blood conservation and graft patency. (8/1215)

The minimal effective dose of aprotinin on hemostasis under normothermic perfusion, the influence of anticoagulant therapy on graft patency, and the thromboembolic and hemorrhagic events were investigated after aortocoronary bypass graft operation (CABG). One hundred CABG patients under normothermic perfusion were randomly divided into the following groups: (1) coumadin plus acetylsalicylic acid (ASA) (n=32); no aprotinin used during cardiopulmonary bypass (CPB); (2) minimal-dose, 10(6) KIU during CPB, aprotinin used, followed by ASA and coumadin (n=36); and (3) very low-dose, total of 2x10(6) KIU before CPB and during CPB; aprotinin used; anticoagulation therapy with heparin early after surgery and followed by replacement with ASA and coumadin (n=32). The patency of arterial grafts was 100% in all groups. The patency of vein grafts was 95-98% and there was no difference among the groups. The blood loss was significantly reduced in both aprotinin groups (groups 2 and 3) compared to the coumadin plus ASA group, although no difference existed between the 2 aprotinin groups. Postoperative thrombotic and hemorrhagic events were not observed in any group. From this study, it was concluded that 10(6) KIU aprotinin in pump-prime-only followed by oral ASA and coumadin was the recommendation from the benefit/cost consideration.  (+info)

Hemostasis is the physiological process that occurs to stop bleeding (bleeding control) when a blood vessel is damaged. This involves the interaction of platelets, vasoconstriction, and blood clotting factors leading to the formation of a clot. The ultimate goal of hemostasis is to maintain the integrity of the vascular system while preventing excessive blood loss.

Surgical hemostasis refers to the methods and techniques used during surgical procedures to stop bleeding or prevent hemorrhage. This can be achieved through various means, including the use of surgical instruments such as clamps, ligatures, or staples to physically compress blood vessels and stop the flow of blood. Electrosurgical tools like cautery may also be used to coagulate and seal off bleeding vessels using heat. Additionally, topical hemostatic agents can be applied to promote clotting and control bleeding in wounded tissues. Effective surgical hemostasis is crucial for ensuring a successful surgical outcome and minimizing the risk of complications such as excessive blood loss, infection, or delayed healing.

Hemostasis, in general, refers to the process of stopping bleeding or hemorrhage, either naturally or through medical intervention. In the context of endoscopy, endoscopic hemostasis is the use of endoscopic techniques and devices to control gastrointestinal (GI) bleeding.

Endoscopes are flexible tubes with a light and camera at the tip, which are inserted into the body to visualize internal organs. In the case of GI endoscopy, the endoscope is inserted through the mouth or rectum to examine the esophagus, stomach, small intestine, large intestine, or rectum.

Endoscopic hemostasis techniques can be broadly categorized into two types:
- Mechanical methods: These involve the use of devices that physically occlude or constrict blood vessels to stop bleeding. Examples include hemoclips, which are metal clips that are deployed through the endoscope to grasp and compress a bleeding vessel, and band ligation, where a rubber band is used to strangulate a bleeding vessel.
- Thermal methods: These use heat to coagulate (seal) blood vessels and stop bleeding. Examples include monopolar and bipolar electrocoagulation, argon plasma coagulation, and laser coagulation.

Endoscopic hemostasis is an important tool in the management of acute GI bleeding, as well as prevention of rebleeding in patients with chronic or recurrent GI bleeding.

Hemostatic techniques refer to various methods used in medicine to stop bleeding or hemorrhage. The goal of these techniques is to promote the body's natural clotting process and prevent excessive blood loss. Some common hemostatic techniques include:

1. Mechanical compression: Applying pressure directly to the wound to physically compress blood vessels and stop the flow of blood. This can be done manually or with the use of medical devices such as clamps, tourniquets, or compression bandages.
2. Suturing or stapling: Closing a wound with stitches or staples to bring the edges of the wound together and allow the body's natural clotting process to occur.
3. Electrocautery: Using heat generated by an electrical current to seal off blood vessels and stop bleeding.
4. Hemostatic agents: Applying topical substances that promote clotting, such as fibrin glue, collagen, or gelatin sponges, to the wound site.
5. Vascular embolization: Inserting a catheter into a blood vessel and injecting a substance that blocks the flow of blood to a specific area, such as a bleeding tumor or aneurysm.
6. Surgical ligation: Tying off a bleeding blood vessel with suture material during surgery.
7. Arterial or venous repair: Repairing damaged blood vessels through surgical intervention to restore normal blood flow and prevent further bleeding.

Hemostatics are substances or agents that promote bleeding cessation or prevent the spread of bleeding. They can act in various ways, such as by stimulating the body's natural clotting mechanisms, constricting blood vessels to reduce blood flow, or forming a physical barrier to block the bleeding site.

Hemostatics are often used in medical settings to manage wounds, injuries, and surgical procedures. They can be applied directly to the wound as a powder, paste, or gauze, or they can be administered systemically through intravenous injection. Examples of hemostatic agents include fibrin sealants, collagen-based products, thrombin, and oxidized regenerated cellulose.

It's important to note that while hemostatics can be effective in controlling bleeding, they should be used with caution and only under the guidance of a healthcare professional. Inappropriate use or overuse of hemostatic agents can lead to complications such as excessive clotting, thrombosis, or tissue damage.

Bleeding time is a medical test that measures the time it takes for a small blood vessel to stop bleeding after being cut. It's used to evaluate platelet function and the effectiveness of blood clotting. The most common method used to measure bleeding time is the Ivy method, which involves making a standardized incision on the forearm and measuring the time it takes for the bleeding to stop. A normal bleeding time ranges from 2 to 9 minutes, but this can vary depending on the specific method used. Prolonged bleeding time may indicate an impairment in platelet function or clotting factor deficiency.

Blood coagulation, also known as blood clotting, is a complex process that occurs in the body to prevent excessive bleeding when a blood vessel is damaged. This process involves several different proteins and chemical reactions that ultimately lead to the formation of a clot.

The coagulation cascade is initiated when blood comes into contact with tissue factor, which is exposed after damage to the blood vessel wall. This triggers a series of enzymatic reactions that activate clotting factors, leading to the formation of a fibrin clot. Fibrin is a protein that forms a mesh-like structure that traps platelets and red blood cells to form a stable clot.

Once the bleeding has stopped, the coagulation process is regulated and inhibited to prevent excessive clotting. The fibrinolytic system degrades the clot over time, allowing for the restoration of normal blood flow.

Abnormalities in the blood coagulation process can lead to bleeding disorders or thrombotic disorders such as deep vein thrombosis and pulmonary embolism.

Blood platelets, also known as thrombocytes, are small, colorless cell fragments in our blood that play an essential role in normal blood clotting. They are formed in the bone marrow from large cells called megakaryocytes and circulate in the blood in an inactive state until they are needed to help stop bleeding. When a blood vessel is damaged, platelets become activated and change shape, releasing chemicals that attract more platelets to the site of injury. These activated platelets then stick together to form a plug, or clot, that seals the wound and prevents further blood loss. In addition to their role in clotting, platelets also help to promote healing by releasing growth factors that stimulate the growth of new tissue.

Thrombosis is the formation of a blood clot (thrombus) inside a blood vessel, obstructing the flow of blood through the circulatory system. When a clot forms in an artery, it can cut off the supply of oxygen and nutrients to the tissues served by that artery, leading to damage or tissue death. If a thrombus forms in the heart, it can cause a heart attack. If a thrombus breaks off and travels through the bloodstream, it can lodge in a smaller vessel, causing blockage and potentially leading to damage in the organ that the vessel supplies. This is known as an embolism.

Thrombosis can occur due to various factors such as injury to the blood vessel wall, abnormalities in blood flow, or changes in the composition of the blood. Certain medical conditions, medications, and lifestyle factors can increase the risk of thrombosis. Treatment typically involves anticoagulant or thrombolytic therapy to dissolve or prevent further growth of the clot, as well as addressing any underlying causes.

Blood coagulation disorders, also known as bleeding disorders or clotting disorders, refer to a group of medical conditions that affect the body's ability to form blood clots properly. Normally, when a blood vessel is injured, the body's coagulation system works to form a clot to stop the bleeding and promote healing.

In blood coagulation disorders, there can be either an increased tendency to bleed due to problems with the formation of clots (hemorrhagic disorder), or an increased tendency for clots to form inappropriately even without injury, leading to blockages in the blood vessels (thrombotic disorder).

Examples of hemorrhagic disorders include:

1. Hemophilia - a genetic disorder that affects the ability to form clots due to deficiencies in clotting factors VIII or IX.
2. Von Willebrand disease - another genetic disorder caused by a deficiency or abnormality of the von Willebrand factor, which helps platelets stick together to form a clot.
3. Liver diseases - can lead to decreased production of coagulation factors, increasing the risk of bleeding.
4. Disseminated intravascular coagulation (DIC) - a serious condition where clotting and bleeding occur simultaneously due to widespread activation of the coagulation system.

Examples of thrombotic disorders include:

1. Factor V Leiden mutation - a genetic disorder that increases the risk of inappropriate blood clot formation.
2. Antithrombin III deficiency - a genetic disorder that impairs the body's ability to break down clots, increasing the risk of thrombosis.
3. Protein C or S deficiencies - genetic disorders that lead to an increased risk of thrombosis due to impaired regulation of the coagulation system.
4. Antiphospholipid syndrome (APS) - an autoimmune disorder where the body produces antibodies against its own clotting factors, increasing the risk of thrombosis.

Treatment for blood coagulation disorders depends on the specific diagnosis and may include medications to manage bleeding or prevent clots, as well as lifestyle changes and monitoring to reduce the risk of complications.

Hemorrhage is defined in the medical context as an excessive loss of blood from the circulatory system, which can occur due to various reasons such as injury, surgery, or underlying health conditions that affect blood clotting or the integrity of blood vessels. The bleeding may be internal, external, visible, or concealed, and it can vary in severity from minor to life-threatening, depending on the location and extent of the bleeding. Hemorrhage is a serious medical emergency that requires immediate attention and treatment to prevent further blood loss, organ damage, and potential death.

Hemostatic disorders are medical conditions that affect the body's ability to stop bleeding (hemorrhage) after an injury or surgery. The hemostatic system includes blood vessels, platelets, and clotting factors that work together to form a clot and prevent further blood loss.

Disorders of hemostasis can be broadly classified into three categories:

1. Bleeding disorders: These are conditions in which the body is unable to form a clot or forms clots that are too weak, leading to excessive bleeding. Examples include hemophilia, von Willebrand disease, and platelet function disorders.
2. Thrombotic disorders: These are conditions in which the body forms clots that are too large or inappropriately located, leading to obstruction of blood flow. Examples include deep vein thrombosis (DVT), pulmonary embolism (PE), and disseminated intravascular coagulation (DIC).
3. Combined disorders: These are conditions in which both bleeding and thrombotic tendencies may be present, depending on the specific circumstances. Examples include antiphospholipid syndrome and thrombotic microangiopathies.

Hemostatic disorders can be inherited or acquired, and their diagnosis and management require a thorough understanding of the underlying pathophysiology and clinical context.

Platelet activation is the process by which platelets (also known as thrombocytes) become biologically active and change from their inactive discoid shape to a spherical shape with pseudopodia, resulting in the release of chemical mediators that are involved in hemostasis and thrombosis. This process is initiated by various stimuli such as exposure to subendothelial collagen, von Willebrand factor, or thrombin during vascular injury, leading to platelet aggregation and the formation of a platelet plug to stop bleeding. Platelet activation also plays a role in inflammation, immune response, and wound healing.

Thromboelastography (TEG) is a viscoelastic method used to assess the kinetics of clot formation, clot strength, and fibrinolysis in whole blood. It provides a global assessment of hemostasis by measuring the mechanical properties of a clot as it forms and dissolves over time. The TEG graph displays several parameters that reflect the different stages of clotting, including reaction time (R), clot formation time (K), angle of clot formation (α), maximum amplitude (MA), and percentage lysis at 30 minutes (LY30). These parameters can help guide transfusion therapy and inform decisions regarding the management of coagulopathy in various clinical settings, such as trauma, cardiac surgery, liver transplantation, and obstetrics.

Blood coagulation factors, also known as clotting factors, are a group of proteins that play a crucial role in the blood coagulation process. They are essential for maintaining hemostasis, which is the body's ability to stop bleeding after injury.

There are 13 known blood coagulation factors, and they are designated by Roman numerals I through XIII. These factors are produced in the liver and are normally present in an inactive form in the blood. When there is an injury to a blood vessel, the coagulation process is initiated, leading to the activation of these factors in a specific order.

The coagulation cascade involves two pathways: the intrinsic and extrinsic pathways. The intrinsic pathway is activated when there is damage to the blood vessel itself, while the extrinsic pathway is activated by tissue factor released from damaged tissues. Both pathways converge at the common pathway, leading to the formation of a fibrin clot.

Blood coagulation factors work together in a complex series of reactions that involve activation, binding, and proteolysis. When one factor is activated, it activates the next factor in the cascade, and so on. This process continues until a stable fibrin clot is formed.

Deficiencies or abnormalities in blood coagulation factors can lead to bleeding disorders such as hemophilia or thrombosis. Hemophilia is a genetic disorder that affects one or more of the coagulation factors, leading to excessive bleeding and difficulty forming clots. Thrombosis, on the other hand, occurs when there is an abnormal formation of blood clots in the blood vessels, which can lead to serious complications such as stroke or pulmonary embolism.

Surgical blood loss is the amount of blood that is lost during a surgical procedure. It can occur through various routes such as incisions, punctures or during the removal of organs or tissues. The amount of blood loss can vary widely depending on the type and complexity of the surgery being performed.

Surgical blood loss can be classified into three categories:

1. Insensible losses: These are small amounts of blood that are lost through the skin, respiratory tract, or gastrointestinal tract during surgery. They are not usually significant enough to cause any clinical effects.
2. Visible losses: These are larger amounts of blood that can be seen and measured directly during surgery. They may require transfusion or other interventions to prevent hypovolemia (low blood volume) and its complications.
3. Hidden losses: These are internal bleeding that cannot be easily seen or measured during surgery. They can occur in the abdominal cavity, retroperitoneal space, or other areas of the body. They may require further exploration or imaging studies to diagnose and manage.

Surgical blood loss can lead to several complications such as hypovolemia, anemia, coagulopathy (disorders of blood clotting), and organ dysfunction. Therefore, it is essential to monitor and manage surgical blood loss effectively to ensure optimal patient outcomes.

Oxidized cellulose is a type of modified cellulose that has undergone oxidation, resulting in the introduction of functional groups such as carboxylic acid or aldehyde groups along the cellulose chain. This process can alter the physical and chemical properties of cellulose, making it more soluble in water and capable of forming gels or films.

Oxidized cellulose is used in a variety of applications, including as a wound dressing material, where it can help to promote healing by providing a moist environment that supports tissue regeneration. It can also be used as a thickening or stabilizing agent in food and cosmetic products, or as a component in the manufacture of specialized papers and textiles.

Platelet aggregation is the clumping together of platelets (thrombocytes) in the blood, which is an essential step in the process of hemostasis (the stopping of bleeding) after injury to a blood vessel. When the inner lining of a blood vessel is damaged, exposure of subendothelial collagen and tissue factor triggers platelet activation. Activated platelets change shape, become sticky, and release the contents of their granules, which include ADP (adenosine diphosphate).

ADP then acts as a chemical mediator to attract and bind additional platelets to the site of injury, leading to platelet aggregation. This forms a plug that seals the damaged vessel and prevents further blood loss. Platelet aggregation is also a crucial component in the formation of blood clots (thrombosis) within blood vessels, which can have pathological consequences such as heart attacks and strokes if they obstruct blood flow to vital organs.

A puncture, in medical terms, refers to a small hole or wound that is caused by a sharp object penetrating the skin or other body tissues. This can result in damage to underlying structures such as blood vessels, nerves, or organs, and may lead to complications such as bleeding, infection, or inflammation.

Punctures can occur accidentally, such as from stepping on a nail or getting pricked by a needle, or they can be inflicted intentionally, such as during medical procedures like injections or blood draws. In some cases, puncture wounds may require medical attention to clean and close the wound, prevent infection, and promote healing.

Peptic ulcer hemorrhage is a medical condition characterized by bleeding in the gastrointestinal tract due to a peptic ulcer. Peptic ulcers are open sores that develop on the lining of the stomach, lower esophagus, or small intestine. They are usually caused by infection with the bacterium Helicobacter pylori or long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs).

When a peptic ulcer bleeds, it can cause symptoms such as vomiting blood or passing black, tarry stools. In severe cases, the bleeding can lead to shock, which is a life-threatening condition characterized by a rapid heartbeat, low blood pressure, and confusion. Peptic ulcer hemorrhage is a serious medical emergency that requires immediate treatment. Treatment may include medications to reduce stomach acid, antibiotics to eliminate H. pylori infection, and endoscopic procedures to stop the bleeding. In some cases, surgery may be necessary to repair the ulcer or remove damaged tissue.

Fibrinogen is a soluble protein present in plasma, synthesized by the liver. It plays an essential role in blood coagulation. When an injury occurs, fibrinogen gets converted into insoluble fibrin by the action of thrombin, forming a fibrin clot that helps to stop bleeding from the injured site. Therefore, fibrinogen is crucial for hemostasis, which is the process of stopping bleeding and starting the healing process after an injury.

Postoperative hemorrhage is a medical term that refers to bleeding that occurs after a surgical procedure. This condition can range from minor oozing to severe, life-threatening bleeding. Postoperative hemorrhage can occur soon after surgery or even several days later, as the surgical site begins to heal.

The causes of postoperative hemorrhage can vary, but some common factors include:

1. Inadequate hemostasis during surgery: This means that all bleeding was not properly controlled during the procedure, leading to bleeding after surgery.
2. Blood vessel injury: During surgery, blood vessels may be accidentally cut or damaged, causing bleeding after the procedure.
3. Coagulopathy: This is a condition in which the body has difficulty forming blood clots, increasing the risk of postoperative hemorrhage.
4. Use of anticoagulant medications: Medications that prevent blood clots can increase the risk of bleeding after surgery.
5. Infection: An infection at the surgical site can cause inflammation and bleeding.

Symptoms of postoperative hemorrhage may include swelling, pain, warmth, or discoloration around the surgical site, as well as signs of shock such as rapid heartbeat, low blood pressure, and confusion. Treatment for postoperative hemorrhage depends on the severity of the bleeding and may include medications to control bleeding, transfusions of blood products, or additional surgery to stop the bleeding.

Hemorrhagic disorders are medical conditions characterized by abnormal bleeding due to impaired blood clotting. This can result from deficiencies in coagulation factors, platelet dysfunction, or the use of medications that interfere with normal clotting processes. Examples include hemophilia, von Willebrand disease, and disseminated intravascular coagulation (DIC). Treatment often involves replacing the missing clotting factor or administering medications to help control bleeding.

A fibrin tissue adhesive is a type of surgical glue that is used to approximate and secure together cut or wounded tissues in the body during surgical procedures. It is made from fibrin, a protein involved in blood clotting, and is often combined with other substances like thrombin and calcium chloride to promote clot formation and enhance adhesion.

Fibrin tissue adhesives work by mimicking the body's natural clotting process. When applied to the wound site, the fibrinogen component of the adhesive is converted into fibrin by the thrombin component, creating a stable fibrin clot that holds the edges of the wound together. This helps to promote healing and reduce the risk of complications such as bleeding or infection.

Fibrin tissue adhesives are commonly used in various surgical procedures, including dermatologic, ophthalmic, orthopedic, and neurologic surgeries. They offer several advantages over traditional suturing methods, such as reduced operation time, less trauma to the tissues, and improved cosmetic outcomes. However, they may not be suitable for all types of wounds or surgical sites, and their use should be determined by a qualified healthcare professional based on individual patient needs and circumstances.

Gastrointestinal (GI) hemorrhage is a term used to describe any bleeding that occurs in the gastrointestinal tract, which includes the esophagus, stomach, small intestine, large intestine, and rectum. The bleeding can range from mild to severe and can produce symptoms such as vomiting blood, passing black or tarry stools, or having low blood pressure.

GI hemorrhage can be classified as either upper or lower, depending on the location of the bleed. Upper GI hemorrhage refers to bleeding that occurs above the ligament of Treitz, which is a point in the small intestine where it becomes narrower and turns a corner. Common causes of upper GI hemorrhage include gastritis, ulcers, esophageal varices, and Mallory-Weiss tears.

Lower GI hemorrhage refers to bleeding that occurs below the ligament of Treitz. Common causes of lower GI hemorrhage include diverticulosis, colitis, inflammatory bowel disease, and vascular abnormalities such as angiodysplasia.

The diagnosis of GI hemorrhage is often made based on the patient's symptoms, medical history, physical examination, and diagnostic tests such as endoscopy, CT scan, or radionuclide scanning. Treatment depends on the severity and cause of the bleeding and may include medications, endoscopic procedures, surgery, or a combination of these approaches.

Thrombin is a serine protease enzyme that plays a crucial role in the coagulation cascade, which is a complex series of biochemical reactions that leads to the formation of a blood clot (thrombus) to prevent excessive bleeding during an injury. Thrombin is formed from its precursor protein, prothrombin, through a process called activation, which involves cleavage by another enzyme called factor Xa.

Once activated, thrombin converts fibrinogen, a soluble plasma protein, into fibrin, an insoluble protein that forms the structural framework of a blood clot. Thrombin also activates other components of the coagulation cascade, such as factor XIII, which crosslinks and stabilizes the fibrin network, and platelets, which contribute to the formation and growth of the clot.

Thrombin has several regulatory mechanisms that control its activity, including feedback inhibition by antithrombin III, a plasma protein that inactivates thrombin and other serine proteases, and tissue factor pathway inhibitor (TFPI), which inhibits the activation of factor Xa, thereby preventing further thrombin formation.

Overall, thrombin is an essential enzyme in hemostasis, the process that maintains the balance between bleeding and clotting in the body. However, excessive or uncontrolled thrombin activity can lead to pathological conditions such as thrombosis, atherosclerosis, and disseminated intravascular coagulation (DIC).

Electrocoagulation is a medical procedure that uses heat generated from an electrical current to cause coagulation (clotting) of tissue. This procedure is often used to treat a variety of medical conditions, such as:

* Gastrointestinal bleeding: Electrocoagulation can be used to control bleeding in the stomach or intestines by applying an electrical current to the affected blood vessels, causing them to shrink and clot.
* Skin lesions: Electrocoagulation can be used to remove benign or malignant skin lesions, such as warts, moles, or skin tags, by applying an electrical current to the growth, which causes it to dehydrate and eventually fall off.
* Vascular malformations: Electrocoagulation can be used to treat vascular malformations (abnormal blood vessels) by applying an electrical current to the affected area, causing the abnormal vessels to shrink and clot.

The procedure is typically performed using a specialized device that delivers an electrical current through a needle or probe. The intensity and duration of the electrical current can be adjusted to achieve the desired effect. Electrocoagulation may be used alone or in combination with other treatments, such as surgery or medication.

It's important to note that electrocoagulation is not without risks, including burns, infection, and scarring. It should only be performed by a qualified medical professional who has experience with the procedure.

Fibrinolysis is the natural process in the body that leads to the dissolution of blood clots. It is a vital part of hemostasis, the process that regulates bleeding and wound healing. Fibrinolysis occurs when plasminogen activators convert plasminogen to plasmin, an enzyme that breaks down fibrin, the insoluble protein mesh that forms the structure of a blood clot. This process helps to prevent excessive clotting and maintains the fluidity of the blood. In medical settings, fibrinolysis can also refer to the therapeutic use of drugs that stimulate this process to dissolve unwanted or harmful blood clots, such as those that cause deep vein thrombosis or pulmonary embolism.

Von Willebrand factor (vWF) is a large multimeric glycoprotein that plays a crucial role in hemostasis, the process which leads to the cessation of bleeding and the formation of a blood clot. It was named after Erik Adolf von Willebrand, a Finnish physician who first described the disorder associated with its deficiency, known as von Willebrand disease (vWD).

The primary functions of vWF include:

1. Platelet adhesion and aggregation: vWF mediates the initial attachment of platelets to damaged blood vessel walls by binding to exposed collagen fibers and then interacting with glycoprotein Ib (GPIb) receptors on the surface of platelets, facilitating platelet adhesion. Subsequently, vWF also promotes platelet-platelet interactions (aggregation) through its interaction with platelet glycoprotein IIb/IIIa (GPIIb/IIIa) receptors under high shear stress conditions found in areas of turbulent blood flow, such as arterioles and the capillary bed.

2. Transport and stabilization of coagulation factor VIII: vWF serves as a carrier protein for coagulation factor VIII (FVIII), protecting it from proteolytic degradation and maintaining its stability in circulation. This interaction between vWF and FVIII is essential for the proper functioning of the coagulation cascade, particularly in the context of vWD, where impaired FVIII function can lead to bleeding disorders.

3. Wound healing: vWF contributes to wound healing by promoting platelet adhesion and aggregation at the site of injury, which facilitates the formation of a provisional fibrin-based clot that serves as a scaffold for tissue repair and regeneration.

In summary, von Willebrand factor is a vital hemostatic protein involved in platelet adhesion, aggregation, coagulation factor VIII stabilization, and wound healing. Deficiencies or dysfunctions in vWF can lead to bleeding disorders such as von Willebrand disease.

Prothrombin time (PT) is a medical laboratory test that measures the time it takes for blood to clot. It's often used to evaluate the functioning of the extrinsic and common pathways of the coagulation system, which is responsible for blood clotting. Specifically, PT measures how long it takes for prothrombin (a protein produced by the liver) to be converted into thrombin, an enzyme that converts fibrinogen into fibrin and helps form a clot.

Prolonged PT may indicate a bleeding disorder or a deficiency in coagulation factors, such as vitamin K deficiency or the use of anticoagulant medications like warfarin. It's important to note that PT is often reported with an international normalized ratio (INR), which allows for standardization and comparison of results across different laboratories and reagent types.

Coagulants are substances that promote the process of coagulation or clotting. They are often used in medical settings to help control bleeding and promote healing. Coagulants work by encouraging the formation of a clot, which helps to stop the flow of blood from a wound or cut.

There are several different types of coagulants that may be used in medical treatments. Some coagulants are naturally occurring substances, such as vitamin K, which is essential for the production of certain clotting factors in the body. Other coagulants may be synthetic or semi-synthetic compounds, such as recombinant activated factor VII (rFVIIa), which is used to treat bleeding disorders and prevent excessive bleeding during surgery.

Coagulants are often administered through injection or infusion, but they can also be applied topically to wounds or cuts. In some cases, coagulants may be used in combination with other treatments, such as compression or cauterization, to help control bleeding and promote healing.

It is important to note that while coagulants can be helpful in controlling bleeding and promoting healing, they can also increase the risk of blood clots and other complications. As a result, they should only be used under the guidance and supervision of a qualified healthcare professional.

Platelet adhesiveness refers to the ability of platelets, which are small blood cells that help your body form clots to prevent excessive bleeding, to stick to other cells or surfaces. This process is crucial in hemostasis, the process of stopping bleeding after injury to a blood vessel.

When the endothelium (the lining of blood vessels) is damaged, subendothelial structures are exposed, which can trigger platelet adhesion. Platelets then change shape and release chemical signals that cause other platelets to clump together, forming a platelet plug. This plug helps to seal the damaged vessel and prevent further bleeding.

Platelet adhesiveness is influenced by several factors, including the presence of von Willebrand factor (vWF), a protein in the blood that helps platelets bind to damaged vessels, and the expression of glycoprotein receptors on the surface of platelets. Abnormalities in platelet adhesiveness can lead to bleeding disorders or thrombotic conditions.

Blood coagulation tests, also known as coagulation studies or clotting tests, are a series of medical tests used to evaluate the blood's ability to clot. These tests measure the functioning of various clotting factors and regulatory proteins involved in the coagulation cascade, which is a complex process that leads to the formation of a blood clot to prevent excessive bleeding.

The most commonly performed coagulation tests include:

1. Prothrombin Time (PT): Measures the time it takes for a sample of plasma to clot after the addition of calcium and tissue factor, which activates the extrinsic pathway of coagulation. The PT is reported in seconds and can be converted to an International Normalized Ratio (INR) to monitor anticoagulant therapy.
2. Activated Partial Thromboplastin Time (aPTT): Measures the time it takes for a sample of plasma to clot after the addition of calcium, phospholipid, and a contact activator, which activates the intrinsic pathway of coagulation. The aPTT is reported in seconds and is used to monitor heparin therapy.
3. Thrombin Time (TT): Measures the time it takes for a sample of plasma to clot after the addition of thrombin, which directly converts fibrinogen to fibrin. The TT is reported in seconds and can be used to detect the presence of fibrin degradation products or abnormalities in fibrinogen function.
4. Fibrinogen Level: Measures the amount of fibrinogen, a protein involved in clot formation, present in the blood. The level is reported in grams per liter (g/L) and can be used to assess bleeding risk or the effectiveness of fibrinogen replacement therapy.
5. D-dimer Level: Measures the amount of D-dimer, a protein fragment produced during the breakdown of a blood clot, present in the blood. The level is reported in micrograms per milliliter (µg/mL) and can be used to diagnose or exclude venous thromboembolism (VTE), such as deep vein thrombosis (DVT) or pulmonary embolism (PE).

These tests are important for the diagnosis, management, and monitoring of various bleeding and clotting disorders. They can help identify the underlying cause of abnormal bleeding or clotting, guide appropriate treatment decisions, and monitor the effectiveness of therapy. It is essential to interpret these test results in conjunction with a patient's clinical presentation and medical history.

Partial Thromboplastin Time (PTT) is a medical laboratory test that measures the time it takes for blood to clot. It's more specifically a measure of the intrinsic and common pathways of the coagulation cascade, which are the series of chemical reactions that lead to the formation of a clot.

The test involves adding a partial thromboplastin reagent (an activator of the intrinsic pathway) and calcium to plasma, and then measuring the time it takes for a fibrin clot to form. This is compared to a control sample, and the ratio of the two times is calculated.

The PTT test is often used to help diagnose bleeding disorders or abnormal blood clotting, such as hemophilia or disseminated intravascular coagulation (DIC). It can also be used to monitor the effectiveness of anticoagulant therapy, such as heparin. Prolonged PTT results may indicate a bleeding disorder or an increased risk of bleeding, while shortened PTT results may indicate a hypercoagulable state and an increased risk of thrombosis.

Thromboplastin is a substance that activates the coagulation cascade, leading to the formation of a clot (thrombus). It's primarily found in damaged or injured tissues and blood vessels, as well as in platelets (thrombocytes). There are two types of thromboplastin:

1. Extrinsic thromboplastin (also known as tissue factor): This is a transmembrane glycoprotein that is primarily found in subendothelial cells and released upon injury to the blood vessels. It initiates the extrinsic pathway of coagulation by binding to and activating Factor VII, ultimately leading to the formation of thrombin and fibrin clots.
2. Intrinsic thromboplastin (also known as plasma thromboplastin or factor III): This term is used less frequently and refers to a labile phospholipid component present in platelet membranes, which plays a role in the intrinsic pathway of coagulation.

In clinical settings, the term "thromboplastin" often refers to reagents used in laboratory tests like the prothrombin time (PT) and activated partial thromboplastin time (aPTT). These reagents contain a source of tissue factor and calcium ions to initiate and monitor the coagulation process.

A gelatin sponge, absorbable is a surgical implant material that is derived from animal collagen. It is prepared in the form of a sterile, compressed sponge which can be expanded with the addition of fluids. The sponge is designed to absorb and hold surgical drainage, promote healing by providing a framework for the growth of new tissue, and then gradually break down and be absorbed by the body over time. It is often used in neurosurgery, plastic surgery, and other surgical specialties for its hemostatic (bleeding control) and supportive properties.

Factor VIIa is a protein involved in the coagulation cascade, which is a series of chemical reactions that leads to the formation of a blood clot. Factor VIIa is the activated form of factor VII, which is normally activated by tissue factor (TF) when there is damage to the blood vessels. Together, TF and Factor VIIa convert Factor X to its active form, Factor Xa, which then converts prothrombin to thrombin, leading to the formation of a fibrin clot.

In summary, Factor VIIa is an important protein in the coagulation cascade that helps to initiate the formation of a blood clot in response to injury.

Surgical instruments are specialized tools or devices that are used by medical professionals during surgical procedures to assist in various tasks such as cutting, dissecting, grasping, holding, retracting, clamping, and suturing body tissues. These instruments are designed to be safe, precise, and effective, with a variety of shapes, sizes, and materials used depending on the specific surgical application. Some common examples of surgical instruments include scalpels, forceps, scissors, hemostats, retractors, and needle holders. Proper sterilization and maintenance of these instruments are crucial to ensure patient safety and prevent infection.

Factor XII deficiency, also known as Hageman factor deficiency, is a rare genetic disorder characterized by a lack or dysfunction of coagulation factor XII. This protein is involved in the initiation of the coagulation cascade, which leads to the formation of a blood clot. People with Factor XII deficiency may have an increased risk of bleeding, but it is typically mild and not life-threatening. The diagnosis is usually made through blood tests that measure the level and function of Factor XII. Treatment is generally not necessary unless there is significant bleeding, in which case fresh frozen plasma or cryoprecipitate may be given to provide temporary correction of the deficiency. It's important to note that Factor XII deficiency is not a common cause of bleeding disorders and it doesn't increase the risk of thrombosis.

Hemophilia A is a genetic bleeding disorder caused by a deficiency in clotting factor VIII. This results in impaired blood clotting and prolonged bleeding, particularly after injuries or surgeries. Symptoms can range from mild to severe, with the most severe form resulting in spontaneous bleeding into joints and muscles, leading to pain, swelling, and potential joint damage over time. Hemophilia A primarily affects males, as it is an X-linked recessive disorder, and is usually inherited from a carrier mother. However, about one third of cases result from a spontaneous mutation in the gene for factor VIII. Treatment typically involves replacement therapy with infusions of factor VIII concentrates to prevent or control bleeding episodes.

Factor VIII is a protein in the blood that is essential for normal blood clotting. It is also known as antihemophilic factor (AHF). Deficiency or dysfunction of this protein results in hemophilia A, a genetic disorder characterized by prolonged bleeding and easy bruising. Factor VIII works together with other proteins to help form a clot and stop bleeding at the site of an injury. It acts as a cofactor for another clotting factor, IX, in the so-called intrinsic pathway of blood coagulation. Intravenous infusions of Factor VIII concentrate are used to treat and prevent bleeding episodes in people with hemophilia A.

Blood coagulation factor inhibitors are substances that interfere with the normal blood clotting process by inhibiting the function of coagulation factors. These inhibitors can be either naturally occurring or artificially produced.

Naturally occurring coagulation factor inhibitors include antithrombin, protein C, and tissue factor pathway inhibitor (TFPI). These inhibitors play a crucial role in regulating the coagulation cascade and preventing excessive clot formation.

Artificially produced coagulation factor inhibitors are used as therapeutic agents to treat thrombotic disorders. Examples include direct oral anticoagulants (DOACs) such as apixaban, rivaroxaban, and dabigatran, which selectively inhibit specific coagulation factors (factor Xa or thrombin).

Additionally, there are also antibodies that can act as coagulation factor inhibitors. These include autoantibodies that develop in some individuals and cause bleeding disorders such as acquired hemophilia A or antiphospholipid syndrome.

A platelet count is a laboratory test that measures the number of platelets, also known as thrombocytes, in a sample of blood. Platelets are small, colorless cell fragments that circulate in the blood and play a crucial role in blood clotting. They help to stop bleeding by sticking together to form a plug at the site of an injured blood vessel.

A normal platelet count ranges from 150,000 to 450,000 platelets per microliter (µL) of blood. A lower than normal platelet count is called thrombocytopenia, while a higher than normal platelet count is known as thrombocytosis.

Abnormal platelet counts can be a sign of various medical conditions, including bleeding disorders, infections, certain medications, and some types of cancer. It is important to consult with a healthcare provider if you have any concerns about your platelet count or if you experience symptoms such as easy bruising, prolonged bleeding, or excessive menstrual flow.

Tissue adhesives, also known as surgical glues or tissue sealants, are medical devices used to approximate and hold together tissues or wounds in place of traditional sutures or staples. They work by creating a bond between the tissue surfaces, helping to promote healing and reduce the risk of infection. Tissue adhesives can be synthetic or biologically derived and are often used in various surgical procedures, including ophthalmic, dermatological, and pediatric surgeries. Some common types of tissue adhesives include cyanoacrylate-based glues, fibrin sealants, and collagen-based sealants.

Factor VII, also known as proconvertin, is a protein involved in the coagulation cascade, which is a series of chemical reactions that leads to the formation of a blood clot. Factor VII is synthesized in the liver and is activated when it comes into contact with tissue factor, which is exposed when blood vessels are damaged. Activated Factor VII then activates Factor X, leading to the formation of thrombin and ultimately a fibrin clot.

Inherited deficiencies or dysfunctions of Factor VII can lead to an increased risk of bleeding, while elevated levels of Factor VII have been associated with an increased risk of thrombosis (blood clots).

Clot retraction is the process that occurs during blood clotting where the platelets in the blood contract and pull together the edges of the clot, causing it to shrink. This process helps to seal off injured blood vessels and prevent further bleeding. Clot retraction also aids in the healing process by helping to remove damaged tissue and debris from the wound site. The proteins in the blood, called fibrin, form a mesh that traps red and white blood cells and platelets, creating a clot. As the platelets contract, they pull on the fibrin mesh, causing it to tighten and the clot to shrink. This process is an important part of the body's natural healing response to injury.

Fibrin is defined as a protein that is formed from fibrinogen during the clotting of blood. It plays an essential role in the formation of blood clots, also known as a clotting or coagulation cascade. When an injury occurs and bleeding starts, fibrin threads form a net-like structure that entraps platelets and red blood cells to create a stable clot, preventing further loss of blood.

The process of forming fibrin from fibrinogen is initiated by thrombin, another protein involved in the coagulation cascade. Thrombin cleaves fibrinogen into fibrin monomers, which then polymerize to form long strands of fibrin. These strands cross-link with each other through a process catalyzed by factor XIIIa, forming a stable clot that protects the wound and promotes healing.

It is important to note that abnormalities in fibrin formation or breakdown can lead to bleeding disorders or thrombotic conditions, respectively. Proper regulation of fibrin production and degradation is crucial for maintaining healthy hemostasis and preventing excessive clotting or bleeding.

The femoral artery is the major blood vessel that supplies oxygenated blood to the lower extremity of the human body. It is a continuation of the external iliac artery and becomes the popliteal artery as it passes through the adductor hiatus in the adductor magnus muscle of the thigh.

The femoral artery is located in the femoral triangle, which is bound by the sartorius muscle anteriorly, the adductor longus muscle medially, and the biceps femoris muscle posteriorly. It can be easily palpated in the groin region, making it a common site for taking blood samples, measuring blood pressure, and performing surgical procedures such as femoral artery catheterization and bypass grafting.

The femoral artery gives off several branches that supply blood to the lower limb, including the deep femoral artery, the superficial femoral artery, and the profunda femoris artery. These branches provide blood to the muscles, bones, skin, and other tissues of the leg, ankle, and foot.

Antithrombin proteins are a type of protein found in the blood that inhibit the formation of blood clots. They work by binding to and neutralizing thrombin and other coagulation factors, such as factor Xa, that are involved in the coagulation cascade. Antithrombin proteins are an important part of the body's natural anticoagulant system, which helps to prevent excessive clotting and maintain proper blood flow.

Antithrombin proteins can be increased through the use of medications such as heparin, which binds to and enhances the activity of antithrombin. This is why heparin is often used as a treatment for conditions associated with abnormal blood clotting, such as deep vein thrombosis or pulmonary embolism.

It's worth noting that while antithrombin proteins are important for preventing excessive clotting, having too few of these proteins can also be a problem, as it can increase the risk of abnormal bleeding.

Von Willebrand disease (vWD) is a genetic bleeding disorder caused by deficiency or dysfunction of the von Willebrand factor (VWF), a protein involved in blood clotting. The VWF plays a crucial role in the formation of a stable platelet plug during the process of hemostasis, which helps to stop bleeding.

There are three main types of vWD:

1. Type 1: This is the most common form, characterized by a partial quantitative deficiency of functional VWF. Bleeding symptoms are usually mild.
2. Type 2: In this type, there is a qualitative defect in the VWF protein leading to various subtypes (2A, 2B, 2M, and 2N) with different bleeding patterns. Symptoms can range from mild to severe.
3. Type 3: This is the most severe form of vWD, characterized by a near or complete absence of functional VWF and Factor VIII. Affected individuals have a high risk of spontaneous and severe bleeding episodes.

The clinical manifestations of vWD include easy bruising, prolonged nosebleeds (epistaxis), heavy menstrual periods in women, and excessive bleeding after dental procedures, surgeries, or trauma. The diagnosis is made based on laboratory tests that assess VWF antigen levels, VWF activity, and Factor VIII coagulant activity. Treatment options include desmopressin (DDAVP) to stimulate the release of VWF from endothelial cells, recombinant VWF, or plasma-derived VWF concentrates, and antifibrinolytic agents like tranexamic acid to reduce bleeding.

Wound closure techniques are methods used to bring the edges of a wound together, allowing for proper healing and minimizing the scar formation. The goal is to approximate the wound edges accurately while providing strength and support to the healing tissues. Several techniques can be employed depending on the type, location, and size of the wound. Some common wound closure techniques include:

1. Sutures (Stitches): A surgical thread is passed through the skin on either side of the wound and tied together to hold the edges in place. Sutures can be absorbable or non-absorbable, and various materials and needle types are used depending on the specific application.
2. Staples: Similar to sutures, staples are used to bring the wound edges together. They are typically faster to apply and remove than sutures, making them suitable for certain types of wounds, such as those on the scalp or torso.
3. Adhesive strips (Steri-Strips): These are thin adhesive bandages applied across the wound to keep the edges approximated. They are often used in conjunction with other closure techniques or for superficial wounds that do not require extensive support.
4. Tissue adhesives (Glues): A liquid adhesive is applied to the wound edges, which then hardens and forms a bond between them. This technique is typically used for minor wounds and can be less invasive than sutures or staples.
5. Skin closure tapes: These are specialized tapes that provide support to the healing wound while also protecting it from external factors. They can be used in combination with other closure techniques or on their own for superficial wounds.
6. Surgical sealants: These are medical-grade materials that create a barrier over the wound, helping to prevent infection and maintain moisture at the wound site. They can be used alongside other closure methods or as an alternative for certain types of wounds.

The choice of wound closure technique depends on various factors, including the location, size, and depth of the wound, patient preferences, and the healthcare provider's expertise. Proper wound care and follow-up are essential to ensure optimal healing and minimize scarring.

Hematology is a branch of medicine that deals with the study of blood, its physiology, and pathophysiology. It involves the diagnosis, treatment, and prevention of diseases related to the blood and blood-forming organs such as the bone marrow, spleen, and lymphatic system. This includes disorders of red and white blood cells, platelets, hemoglobin, blood vessels, and coagulation (blood clotting). Some common hematological diseases include anemia, leukemia, lymphoma, sickle cell disease, and bleeding disorders like hemophilia.

Disseminated Intravascular Coagulation (DIC) is a complex medical condition characterized by the abnormal activation of the coagulation cascade, leading to the formation of blood clots in small blood vessels throughout the body. This process can result in the consumption of clotting factors and platelets, which can then lead to bleeding complications. DIC can be caused by a variety of underlying conditions, including sepsis, trauma, cancer, and obstetric emergencies.

The term "disseminated" refers to the widespread nature of the clotting activation, while "intravascular" indicates that the clotting is occurring within the blood vessels. The condition can manifest as both bleeding and clotting complications, which can make it challenging to diagnose and manage.

The diagnosis of DIC typically involves laboratory tests that evaluate coagulation factors, platelet count, fibrin degradation products, and other markers of coagulation activation. Treatment is focused on addressing the underlying cause of the condition while also managing any bleeding or clotting complications that may arise.

Antithrombin III is a protein that inhibits the formation of blood clots (thrombi) in the body. It does this by inactivating several enzymes involved in coagulation, including thrombin and factor Xa. Antithrombin III is produced naturally by the liver and is also available as a medication for the prevention and treatment of thromboembolic disorders, such as deep vein thrombosis and pulmonary embolism. It works by binding to and neutralizing excess clotting factors in the bloodstream, thereby reducing the risk of clot formation.

Anticoagulants are a class of medications that work to prevent the formation of blood clots in the body. They do this by inhibiting the coagulation cascade, which is a series of chemical reactions that lead to the formation of a clot. Anticoagulants can be given orally, intravenously, or subcutaneously, depending on the specific drug and the individual patient's needs.

There are several different types of anticoagulants, including:

1. Heparin: This is a naturally occurring anticoagulant that is often used in hospitalized patients who require immediate anticoagulation. It works by activating an enzyme called antithrombin III, which inhibits the formation of clots.
2. Low molecular weight heparin (LMWH): LMWH is a form of heparin that has been broken down into smaller molecules. It has a longer half-life than standard heparin and can be given once or twice daily by subcutaneous injection.
3. Direct oral anticoagulants (DOACs): These are newer oral anticoagulants that work by directly inhibiting specific clotting factors in the coagulation cascade. Examples include apixaban, rivaroxaban, and dabigatran.
4. Vitamin K antagonists: These are older oral anticoagulants that work by inhibiting the action of vitamin K, which is necessary for the formation of clotting factors. Warfarin is an example of a vitamin K antagonist.

Anticoagulants are used to prevent and treat a variety of conditions, including deep vein thrombosis (DVT), pulmonary embolism (PE), atrial fibrillation, and prosthetic heart valve thrombosis. It is important to note that anticoagulants can increase the risk of bleeding, so they must be used with caution and regular monitoring of blood clotting times may be required.

Fibrin(ogen) degradation products (FDPs) are a group of proteins that result from the breakdown of fibrinogen and fibrin, which are key components of blood clots. This process occurs during the normal physiological process of fibrinolysis, where clots are dissolved to maintain blood flow.

FDPs can be measured in the blood as a marker for the activation of the coagulation and fibrinolytic systems. Elevated levels of FDPs may indicate the presence of a disorder that causes abnormal clotting or bleeding, such as disseminated intravascular coagulation (DIC), deep vein thrombosis (DVT), pulmonary embolism (PE), or certain types of cancer.

It is important to note that FDPs are not specific to any particular disorder and their measurement should be interpreted in conjunction with other clinical and laboratory findings.

Platelet membrane glycoproteins are specialized proteins found on the surface of platelets, which are small blood cells responsible for clotting. These glycoproteins play crucial roles in various processes related to hemostasis and thrombosis, including platelet adhesion, activation, and aggregation.

There are several key platelet membrane glycoproteins, such as:

1. Glycoprotein (GP) Ia/IIa (also known as integrin α2β1): This glycoprotein mediates the binding of platelets to collagen fibers in the extracellular matrix, facilitating platelet adhesion and activation.
2. GP IIb/IIIa (also known as integrin αIIbβ3): This is the most abundant glycoprotein on the platelet surface and functions as a receptor for fibrinogen, von Willebrand factor, and other adhesive proteins. Upon activation, GP IIb/IIIa undergoes conformational changes that enable it to bind these ligands, leading to platelet aggregation and clot formation.
3. GPIb-IX-V: This glycoprotein complex is involved in the initial tethering and adhesion of platelets to von Willebrand factor (vWF) in damaged blood vessels. It consists of four subunits: GPIbα, GPIbβ, GPIX, and GPV.
4. GPVI: This glycoprotein is essential for platelet activation upon contact with collagen. It associates with the Fc receptor γ-chain (FcRγ) to form a signaling complex that triggers intracellular signaling pathways, leading to platelet activation and aggregation.

Abnormalities in these platelet membrane glycoproteins can lead to bleeding disorders or thrombotic conditions. For example, mutations in GPIIb/IIIa can result in Glanzmann's thrombasthenia, a severe bleeding disorder characterized by impaired platelet aggregation. On the other hand, increased expression or activation of these glycoproteins may contribute to the development of arterial thrombosis and cardiovascular diseases.

Fibrin foam is not a widely recognized medical term, but it does refer to a type of biocompatible material that is used in certain medical and surgical applications.

Fibrin is a protein involved in the clotting of blood, and fibrin foam is created by combining fibrin with a foaming agent to create a porous structure. The resulting material can be used as a scaffold for tissue regeneration or as a filler in surgical procedures.

In some cases, fibrin foam may also be impregnated with various growth factors or other therapeutic agents to promote healing and tissue repair. The use of fibrin foam has been explored in a variety of clinical settings, including wound healing, bone regeneration, and the treatment of soft tissue defects.

The platelet glycoprotein GPIb-IX complex is a crucial receptor on the surface of platelets that plays a vital role in hemostasis and thrombosis. It is a heterotetrameric transmembrane protein complex composed of two disulfide-linked glycoprotein subunits, GPIbα, GPIbβ, GPV (Glycoprotein V), and GPIX (Glycoprotein IX).

The GPIb-IX complex is responsible for the initial interaction between platelets and von Willebrand factor (vWF) in the circulation. When blood vessels are damaged, exposed collagen recruits vWF to the site of injury, where it binds to the GPIbα subunit of the GPIb-IX complex, leading to platelet adhesion and activation. This interaction is critical for primary hemostasis, which helps prevent excessive blood loss from injured vessels.

Genetic mutations or deficiencies in the genes encoding these glycoproteins can lead to bleeding disorders such as Bernard-Soulier syndrome, a rare autosomal recessive disorder characterized by thrombocytopenia and large platelets with impaired vWF binding and platelet adhesion.

Prothrombin is a protein present in blood plasma, and it's also known as coagulation factor II. It plays a crucial role in the coagulation cascade, which is a complex series of reactions that leads to the formation of a blood clot.

When an injury occurs, the coagulation cascade is initiated to prevent excessive blood loss. Prothrombin is converted into its active form, thrombin, by another factor called factor Xa in the presence of calcium ions, phospholipids, and factor Va. Thrombin then catalyzes the conversion of fibrinogen into fibrin, forming a stable clot.

Prothrombin levels can be measured through a blood test, which is often used to diagnose or monitor conditions related to bleeding or coagulation disorders, such as liver disease or vitamin K deficiency.

I apologize for any confusion, but "Enbucrilate" is not a medical term or a medication that I am aware of. It's possible that there might be some misunderstanding or misspelling in the term. If you have more context or information about where this term came from, I may be able to provide a more accurate and helpful response.

However, if you are referring to "bucrilate" which is a type of polymer used in some medical applications such as wound dressings, then it is a substance that can absorb large amounts of water and create a gel-like barrier between the wound and the outside environment, helping to keep the wound moist and promote healing.

If you have any further questions or concerns, please don't hesitate to ask.

Factor XI deficiency, also known as Hemophilia C or Rosenthal syndrome, is a rare bleeding disorder caused by a deficiency or dysfunction of coagulation factor XI. This protease plays an important role in the intrinsic pathway of blood coagulation. Factor XI deficiency can lead to prolonged bleeding after surgery, trauma, or menstruation, but it typically does not cause spontaneous bleeding like Hemophilia A and B. The severity of the condition varies widely among affected individuals. Inheritance is autosomal recessive, meaning that two defective copies of the gene (one from each parent) are necessary to have the disease.

Coagulation protein disorders are a group of medical conditions that affect the body's ability to form blood clots properly. These disorders can be caused by genetic defects or acquired factors, such as liver disease or vitamin K deficiency.

The coagulation system is a complex process that involves various proteins called clotting factors. When there is an injury to a blood vessel, these clotting factors work together in a specific order to form a clot and prevent excessive bleeding. In coagulation protein disorders, one or more of these clotting factors are missing or not functioning properly, leading to abnormal bleeding or clotting.

There are several types of coagulation protein disorders, including:

1. Hemophilia: This is a genetic disorder that affects the clotting factor VIII or IX. People with hemophilia may experience prolonged bleeding after injuries, surgery, or dental work.
2. Von Willebrand disease: This is another genetic disorder that affects the von Willebrand factor, a protein that helps platelets stick together and form a clot. People with this condition may have nosebleeds, easy bruising, and excessive bleeding during menstruation or after surgery.
3. Factor XI deficiency: This is a rare genetic disorder that affects the clotting factor XI. People with this condition may experience prolonged bleeding after surgery or trauma.
4. Factor VII deficiency: This is a rare genetic disorder that affects the clotting factor VII. People with this condition may have nosebleeds, easy bruising, and excessive bleeding during menstruation or after surgery.
5. Acquired coagulation protein disorders: These are conditions that develop due to other medical factors, such as liver disease, vitamin K deficiency, or the use of certain medications. These disorders can affect one or more clotting factors and may cause abnormal bleeding or clotting.

Treatment for coagulation protein disorders depends on the specific condition and severity of symptoms. In some cases, replacement therapy with the missing clotting factor may be necessary to prevent excessive bleeding. Other treatments may include medications to control bleeding, such as desmopressin or antifibrinolytic agents, and lifestyle changes to reduce the risk of injury and bleeding.

Suture techniques refer to the various methods used by surgeons to sew or stitch together tissues in the body after an injury, trauma, or surgical incision. The main goal of suturing is to approximate and hold the edges of the wound together, allowing for proper healing and minimizing scar formation.

There are several types of suture techniques, including:

1. Simple Interrupted Suture: This is one of the most basic suture techniques where the needle is passed through the tissue at a right angle, creating a loop that is then tightened to approximate the wound edges. Multiple stitches are placed along the length of the incision or wound.
2. Continuous Locking Suture: In this technique, the needle is passed continuously through the tissue in a zigzag pattern, with each stitch locking into the previous one. This creates a continuous line of sutures that provides strong tension and support to the wound edges.
3. Running Suture: Similar to the continuous locking suture, this technique involves passing the needle continuously through the tissue in a straight line. However, instead of locking each stitch, the needle is simply passed through the previous loop before being tightened. This creates a smooth and uninterrupted line of sutures that can be easily removed after healing.
4. Horizontal Mattress Suture: In this technique, two parallel stitches are placed horizontally across the wound edges, creating a "mattress" effect that provides additional support and tension to the wound. This is particularly useful in deep or irregularly shaped wounds.
5. Vertical Mattress Suture: Similar to the horizontal mattress suture, this technique involves placing two parallel stitches vertically across the wound edges. This creates a more pronounced "mattress" effect that can help reduce tension and minimize scarring.
6. Subcuticular Suture: In this technique, the needle is passed just below the surface of the skin, creating a smooth and barely visible line of sutures. This is particularly useful in cosmetic surgery or areas where minimizing scarring is important.

The choice of suture technique depends on various factors such as the location and size of the wound, the type of tissue involved, and the patient's individual needs and preferences. Proper suture placement and tension are crucial for optimal healing and aesthetic outcomes.

Occlusive dressings are specialized bandages or coverings that form a barrier over the skin, preventing air and moisture from passing through. They are designed to create a moist environment that promotes healing by increasing local blood flow, reducing wound desiccation, and encouraging the growth of new tissue. Occlusive dressings can also help to minimize pain, scarring, and the risk of infection in wounds. These dressings are often used for dry, necrotic, or hard-to-heal wounds, such as pressure ulcers, diabetic foot ulcers, and burns. It is important to monitor the wound closely while using occlusive dressings, as they can sometimes lead to skin irritation or maceration if left in place for too long.

A hematoma is defined as a localized accumulation of blood in a tissue, organ, or body space caused by a break in the wall of a blood vessel. This can result from various causes such as trauma, surgery, or certain medical conditions that affect coagulation. The severity and size of a hematoma may vary depending on the location and extent of the bleeding. Symptoms can include swelling, pain, bruising, and decreased mobility in the affected area. Treatment options depend on the size and location of the hematoma but may include observation, compression, ice, elevation, or in some cases, surgical intervention.

Surgical tampons are medical devices that are used to pack or plug a cavity or wound in the body during surgical procedures. They are typically made of gauze, rayon, or synthetic materials and come in various shapes and sizes to accommodate different surgical needs. Surgical tampons can help control bleeding, prevent the accumulation of fluids, and maintain the position of organs or tissues during surgery. After the procedure, they are usually removed or allowed to dissolve naturally. It is important to note that surgical tampons should not be confused with feminine hygiene tampons used for menstruation.

Gastrointestinal endoscopy is a medical procedure that allows direct visualization of the inner lining of the digestive tract, which includes the esophagus, stomach, small intestine, large intestine (colon), and sometimes the upper part of the small intestine (duodenum). This procedure is performed using an endoscope, a long, thin, flexible tube with a light and camera at its tip. The endoscope is inserted through the mouth for upper endoscopy or through the rectum for lower endoscopy (colonoscopy), and the images captured by the camera are transmitted to a monitor for the physician to view.

Gastrointestinal endoscopy can help diagnose various conditions, such as inflammation, ulcers, tumors, polyps, or bleeding in the digestive tract. It can also be used for therapeutic purposes, such as removing polyps, taking tissue samples (biopsies), treating bleeding, and performing other interventions to manage certain digestive diseases.

There are different types of gastrointestinal endoscopy procedures, including:

1. Upper Endoscopy (Esophagogastroduodenoscopy or EGD): This procedure examines the esophagus, stomach, and duodenum.
2. Colonoscopy: This procedure examines the colon and rectum.
3. Sigmoidoscopy: A limited examination of the lower part of the colon (sigmoid colon) using a shorter endoscope.
4. Enteroscopy: An examination of the small intestine, which can be performed using various techniques, such as push enteroscopy, single-balloon enteroscopy, or double-balloon enteroscopy.
5. Capsule Endoscopy: A procedure that involves swallowing a small capsule containing a camera, which captures images of the digestive tract as it passes through.

Gastrointestinal endoscopy is generally considered safe when performed by experienced medical professionals. However, like any medical procedure, there are potential risks and complications, such as bleeding, infection, perforation, or adverse reactions to sedatives used during the procedure. Patients should discuss these risks with their healthcare provider before undergoing gastrointestinal endoscopy.

Platelet function tests are laboratory tests that measure how well platelets, which are small blood cells responsible for clotting, function in preventing or stopping bleeding. These tests are often used to investigate the cause of abnormal bleeding or bruising, or to monitor the effectiveness of antiplatelet therapy in patients with certain medical conditions such as heart disease or stroke.

There are several types of platelet function tests available, including:

1. Platelet count: This test measures the number of platelets present in a sample of blood. A low platelet count can increase the risk of bleeding.
2. Bleeding time: This test measures how long it takes for a small cut to stop bleeding. It is used less frequently than other tests due to its invasiveness and variability.
3. Platelet aggregation tests: These tests measure how well platelets clump together (aggregate) in response to various agents that promote platelet activation, such as adenosine diphosphate (ADP), collagen, or epinephrine.
4. Platelet function analyzer (PFA): This test measures the time it takes for a blood sample to clot under shear stress, simulating the conditions in an injured blood vessel. The PFA can provide information about the overall platelet function and the effectiveness of antiplatelet therapy.
5. Thromboelastography (TEG) or rotational thromboelastometry (ROTEM): These tests measure the kinetics of clot formation, strength, and dissolution in whole blood samples. They provide information about both platelet function and coagulation factors.

These tests can help healthcare providers diagnose bleeding disorders, assess the risk of bleeding during surgery or other invasive procedures, monitor antiplatelet therapy, and guide treatment decisions for patients with abnormal platelet function.

The platelet glycoprotein GPIIb-IIIa complex, also known as integrin αIIbβ3 or CD41/CD61, is a heterodimeric transmembrane receptor found on the surface of platelets and megakaryocytes. It plays a crucial role in platelet aggregation and thrombus formation during hemostasis and pathological conditions such as arterial thrombosis.

The GPIIb-IIIa complex is composed of two non-covalently associated subunits, GPIIb (αIIb or CD41) and IIIa (β3 or CD61). Upon platelet activation by various agonists like ADP, thrombin, or collagen, the GPIIb-IIIa complex undergoes a conformational change that allows it to bind fibrinogen, von Willebrand factor, and other adhesive proteins. This binding event leads to platelet aggregation and the formation of a hemostatic plug or pathological thrombus.

Inhibition of the GPIIb-IIIa complex has been a target for antiplatelet therapy in the prevention and treatment of arterial thrombosis, such as myocardial infarction and stroke. Several pharmacological agents, including monoclonal antibodies and small molecule antagonists, have been developed to block this complex and reduce platelet aggregation.

Megakaryocytes are large, specialized bone marrow cells that are responsible for the production and release of platelets (also known as thrombocytes) into the bloodstream. Platelets play an essential role in blood clotting and hemostasis, helping to prevent excessive bleeding during injuries or trauma.

Megakaryocytes have a unique structure with multilobed nuclei and abundant cytoplasm rich in organelles called alpha-granules and dense granules, which store various proteins, growth factors, and enzymes necessary for platelet function. As megakaryocytes mature, they extend long cytoplasmic processes called proplatelets into the bone marrow sinuses, where these extensions fragment into individual platelets that are released into circulation.

Abnormalities in megakaryocyte number, size, or function can lead to various hematological disorders, such as thrombocytopenia (low platelet count), thrombocytosis (high platelet count), and certain types of leukemia.

Factor XI, also known as plasma thromboplastin antecedent (PTA) or antihemophilic factor C, is a protein involved in blood coagulation. It is one of the factors in the intrinsic pathway of coagulation, which is activated when blood comes into contact with negatively charged surfaces, such as damaged blood vessels.

When Factor XI is activated (usually by thrombin or activated Factor XII), it activates more Factor XI and also activates Factor IX, leading to the formation of a complex that converts Factor X to its active form, Factor Xa. This ultimately leads to the formation of a fibrin clot and helps to stop bleeding.

Deficiencies in Factor XI can lead to an increased risk of bleeding, although the severity of the bleeding disorder can vary widely among individuals with Factor XI deficiency. Treatment for Factor XI deficiency typically involves replacement therapy with fresh frozen plasma or recombinant Factor XI concentrate.

Glycoprotein IIb (also known as integrin αIIbβ3 or CD41/CD61) is a type of protein found on the surface of platelets, which are small cell fragments involved in blood clotting. This glycoprotein plays a crucial role in the final pathway of platelet activation and aggregation, which ultimately leads to the formation of a clot to stop bleeding.

More specifically, Glycoprotein IIb is responsible for binding fibrinogen, von Willebrand factor, and other adhesive proteins in the blood, allowing platelets to bind together and form a clot. Mutations or defects in this glycoprotein can lead to bleeding disorders such as Glanzmann thrombasthenia, which is characterized by abnormal platelet function and excessive bleeding.

Fibrinopeptide A is a small protein molecule that is cleaved and released from the larger fibrinogen protein during the blood clotting process. Specifically, it is removed by the enzyme thrombin as part of the conversion of fibrinogen to fibrin, which is the main structural component of a blood clot. The measurement of Fibrinopeptide A in the blood can be used as a marker for ongoing thrombin activation and fibrin formation, which are key events in coagulation and hemostasis. Increased levels of Fibrinopeptide A may indicate abnormal or excessive blood clotting, such as in disseminated intravascular coagulation (DIC) or deep vein thrombosis (DVT).

Cyanoacrylates are a type of fast-acting adhesive that polymerize in the presence of moisture. They are commonly used in medical settings as tissue adhesives or surgical glues to close wounds and promote healing. The most well-known cyanoacrylate is probably "super glue," which is not intended for medical use.

In a medical context, cyanoacrylates are often used as an alternative to sutures or staples to close minor cuts and wounds. They can also be used in certain surgical procedures to help stop bleeding and hold tissue together while it heals. The adhesive forms a strong bond that helps to keep the wound closed and reduce the risk of infection.

It's important to note that cyanoacrylates should only be used under the direction of a healthcare professional, as improper use can lead to skin irritation or other complications. Additionally, cyanoacrylates are not suitable for all types of wounds, so it's important to follow your doctor's instructions carefully when using these products.

Treatment outcome is a term used to describe the result or effect of medical treatment on a patient's health status. It can be measured in various ways, such as through symptoms improvement, disease remission, reduced disability, improved quality of life, or survival rates. The treatment outcome helps healthcare providers evaluate the effectiveness of a particular treatment plan and make informed decisions about future care. It is also used in clinical research to compare the efficacy of different treatments and improve patient care.

Proteinase-activated receptors (PARs) are a subfamily of G protein-coupled receptors that are activated by proteolytic cleavage of their extracellular N-terminal domain. This process exposes a new tethered ligand domain that binds to the receptor and activates it.

There are four known PARs (PAR-1, PAR-2, PAR-3, and PAR-4) that play important roles in various physiological and pathophysiological processes, including inflammation, hemostasis, wound healing, and cancer. Proteinases such as thrombin, trypsin, and matrix metalloproteinases can activate PARs, leading to the activation of downstream signaling pathways that regulate cellular responses such as proliferation, migration, and gene expression.

Proteinase-activated receptors have been identified as important drug targets for various diseases, including thrombosis, inflammation, and cancer. Inhibitors or antagonists of PARs have shown promise in preclinical and clinical studies for the treatment of these conditions.

Hemophilia B is a genetic disorder that affects the body's ability to control blood clotting, also known as coagulation. This condition is caused by a deficiency or dysfunction in Factor IX, one of the proteins essential for normal blood clotting. As a result, people with Hemophilia B experience prolonged bleeding and bruising after injuries, surgeries, or spontaneously, particularly in joints and muscles.

There are different degrees of severity, depending on how much Factor IX is missing or not functioning properly. Mild cases may only become apparent after significant trauma, surgery, or tooth extraction, while severe cases can lead to spontaneous bleeding into joints and muscles, causing pain, swelling, and potential long-term damage. Hemophilia B primarily affects males, as it is an X-linked recessive disorder, but females can be carriers of the condition and may experience mild symptoms.

A false aneurysm, also known as a pseudoaneurysm, is a type of aneurysm that occurs when there is a leakage or rupture of blood from a blood vessel into the surrounding tissues, creating a pulsating hematoma or collection of blood. Unlike true aneurysms, which involve a localized dilation or bulging of the blood vessel wall, false aneurysms do not have a complete covering of all three layers of the arterial wall (intima, media, and adventitia). Instead, they are typically covered by only one or two layers, such as the intima and adventitia, or by surrounding tissues like connective tissue or fascia.

False aneurysms can result from various factors, including trauma, infection, iatrogenic causes (such as medical procedures), or degenerative changes in the blood vessel wall. They are more common in arteries than veins and can occur in any part of the body. If left untreated, false aneurysms can lead to serious complications such as rupture, thrombosis, distal embolization, or infection. Treatment options for false aneurysms include surgical repair, endovascular procedures, or observation with regular follow-up imaging.

Factor Xa is a serine protease that plays a crucial role in the coagulation cascade, which is a series of reactions that lead to the formation of a blood clot. It is one of the activated forms of Factor X, a pro-protein that is converted to Factor Xa through the action of other enzymes in the coagulation cascade.

Factor Xa functions as a key component of the prothrombinase complex, which also includes calcium ions, phospholipids, and activated Factor V (also known as Activated Protein C or APC). This complex is responsible for converting prothrombin to thrombin, which then converts fibrinogen to fibrin, forming a stable clot.

Inhibitors of Factor Xa are used as anticoagulants in the prevention and treatment of thromboembolic disorders such as deep vein thrombosis and pulmonary embolism. These drugs work by selectively inhibiting Factor Xa, thereby preventing the formation of the prothrombinase complex and reducing the risk of clot formation.

A platelet transfusion is the process of medically administering platelets, which are small blood cells that help your body form clots to stop bleeding. Platelet transfusions are often given to patients with low platelet counts or dysfunctional platelets due to various reasons such as chemotherapy, bone marrow transplantation, disseminated intravascular coagulation (DIC), and other medical conditions leading to increased consumption or destruction of platelets. This procedure helps to prevent or treat bleeding complications in these patients. It's important to note that platelet transfusions should be given under the supervision of a healthcare professional, taking into account the patient's clinical condition, platelet count, and potential risks associated with transfusion reactions.

Desmopressin, also known as 1-deamino-8-D-arginine vasopressin (dDAVP), is a synthetic analogue of the natural hormone arginine vasopressin. It is commonly used in medical practice for the treatment of diabetes insipidus, a condition characterized by excessive thirst and urination due to lack of antidiuretic hormone (ADH).

Desmopressin works by binding to V2 receptors in the kidney, which leads to increased water reabsorption and reduced urine production. It also has some effect on V1 receptors, leading to vasoconstriction and increased blood pressure. However, its primary use is for its antidiuretic effects.

In addition to its use in diabetes insipidus, desmopressin may also be used to treat bleeding disorders such as hemophilia and von Willebrand disease, as it can help to promote platelet aggregation and reduce bleeding times. It is available in various forms, including nasal sprays, injectable solutions, and oral tablets or dissolvable films.

Factor XII, also known as Hageman factor, is a protein that plays a role in the coagulation cascade, which is the series of events that leads to the formation of a blood clot. It is one of the zymogens, or inactive precursor proteins, that becomes activated and helps to trigger the coagulation process.

When Factor XII comes into contact with negatively charged surfaces, such as damaged endothelial cells or artificial surfaces like those found on medical devices, it undergoes a conformational change and becomes activated. Activated Factor XII then activates other proteins in the coagulation cascade, including Factor XI, which ultimately leads to the formation of a fibrin clot.

Deficiencies in Factor XII are generally not associated with bleeding disorders, as the coagulation cascade can still proceed through other pathways. However, excessive activation of Factor XII has been implicated in certain thrombotic disorders, such as deep vein thrombosis and disseminated intravascular coagulation (DIC).

Protein C is a vitamin K-dependent protease that functions as an important regulator of coagulation and inflammation. It is a plasma protein produced in the liver that, when activated, degrades clotting factors Va and VIIIa to limit thrombus formation and prevent excessive blood clotting. Protein C also has anti-inflammatory properties by inhibiting the release of pro-inflammatory cytokines and reducing endothelial cell activation. Inherited or acquired deficiencies in Protein C can lead to an increased risk of thrombosis, a condition characterized by abnormal blood clot formation within blood vessels.

Weibel-Palade bodies are rod-shaped, membrane-bound organelles found in the cytoplasm of endothelial cells, which line the interior surface of blood vessels. They were first described by Edwin Weibel and George Palade in 1964. These organelles are unique to endothelial cells and serve as storage sites for von Willebrand factor (vWF) and other proteins involved in hemostasis, inflammation, and vasomotor functions.

The main components of Weibel-Palade bodies include:

1. Von Willebrand factor (vWF): A multimeric glycoprotein that plays a crucial role in platelet adhesion and aggregation at the site of vascular injury, as well as mediating the transport of coagulation factors VIII and V.
2. P-selectin: A cell adhesion molecule that facilitates leukocyte rolling and recruitment to sites of inflammation.
3. Endothelial nitric oxide synthase (eNOS): An enzyme responsible for the production of nitric oxide, a potent vasodilator that regulates vascular tone and blood flow.
4. Angiopoietin-2: A growth factor involved in angiogenesis and vascular remodeling.
5. Tissue plasminogen activator (tPA): A serine protease that plays a role in fibrinolysis, the process of breaking down blood clots.

Upon stimulation by various agonists such as thrombin, histamine, or vascular endothelial growth factor (VEGF), Weibel-Palade bodies undergo exocytosis, releasing their contents into the extracellular space. This process contributes to hemostatic responses, inflammatory reactions, and modulation of vascular tone.

Platelet aggregation inhibitors are a class of medications that prevent platelets (small blood cells involved in clotting) from sticking together and forming a clot. These drugs work by interfering with the ability of platelets to adhere to each other and to the damaged vessel wall, thereby reducing the risk of thrombosis (blood clot formation).

Platelet aggregation inhibitors are often prescribed for people who have an increased risk of developing blood clots due to various medical conditions such as atrial fibrillation, coronary artery disease, peripheral artery disease, stroke, or a history of heart attack. They may also be used in patients undergoing certain medical procedures, such as angioplasty and stenting, to prevent blood clot formation in the stents.

Examples of platelet aggregation inhibitors include:

1. Aspirin: A nonsteroidal anti-inflammatory drug (NSAID) that irreversibly inhibits the enzyme cyclooxygenase, which is involved in platelet activation and aggregation.
2. Clopidogrel (Plavix): A P2Y12 receptor antagonist that selectively blocks ADP-induced platelet activation and aggregation.
3. Prasugrel (Effient): A third-generation thienopyridine P2Y12 receptor antagonist, similar to clopidogrel but with faster onset and greater potency.
4. Ticagrelor (Brilinta): A direct-acting P2Y12 receptor antagonist that does not require metabolic activation and has a reversible binding profile.
5. Dipyridamole (Persantine): An antiplatelet agent that inhibits platelet aggregation by increasing cyclic adenosine monophosphate (cAMP) levels in platelets, which leads to decreased platelet reactivity.
6. Iloprost (Ventavis): A prostacyclin analogue that inhibits platelet aggregation and causes vasodilation, often used in the treatment of pulmonary arterial hypertension.
7. Cilostazol (Pletal): A phosphodiesterase III inhibitor that increases cAMP levels in platelets, leading to decreased platelet activation and aggregation, as well as vasodilation.
8. Ticlopidine (Ticlid): An older P2Y12 receptor antagonist with a slower onset of action and more frequent side effects compared to clopidogrel or prasugrel.

Protein S is a vitamin K-dependent protein found in the blood that functions as a natural anticoagulant. It plays a crucial role in regulating the body's clotting system by inhibiting the activation of coagulation factors, thereby preventing excessive blood clotting. Protein S also acts as a cofactor for activated protein C, which is another important anticoagulant protein.

Protein S exists in two forms: free and bound to a protein called C4b-binding protein (C4BP). Only the free form of Protein S has biological activity in inhibiting coagulation. Inherited or acquired deficiencies in Protein S can lead to an increased risk of thrombosis, or abnormal blood clot formation, which can cause various medical conditions such as deep vein thrombosis (DVT) and pulmonary embolism (PE). Regular monitoring of Protein S levels is essential for patients with a history of thrombotic events or those who have a family history of thrombophilia.

Antithrombins are substances that prevent the formation or promote the dissolution of blood clots (thrombi). They include:

1. Anticoagulants: These are medications that reduce the ability of the blood to clot. Examples include heparin, warfarin, and direct oral anticoagulants (DOACs) such as apixaban, rivaroxaban, and dabigatran.
2. Thrombolytic agents: These are medications that break down existing blood clots. Examples include alteplase, reteplase, and tenecteplase.
3. Fibrinolytics: These are a type of thrombolytic agent that specifically target fibrin, a protein involved in the formation of blood clots.
4. Natural anticoagulants: These are substances produced by the body to regulate blood clotting. Examples include antithrombin III, protein C, and protein S.

Antithrombins are used in the prevention and treatment of various thromboembolic disorders, such as deep vein thrombosis (DVT), pulmonary embolism (PE), stroke, and myocardial infarction (heart attack). It is important to note that while antithrombins can help prevent or dissolve blood clots, they also increase the risk of bleeding, so their use must be carefully monitored.

Thrombocytopenia is a medical condition characterized by an abnormally low platelet count (thrombocytes) in the blood. Platelets are small cell fragments that play a crucial role in blood clotting, helping to stop bleeding when a blood vessel is damaged. A healthy adult typically has a platelet count between 150,000 and 450,000 platelets per microliter of blood. Thrombocytopenia is usually diagnosed when the platelet count falls below 150,000 platelets/µL.

Thrombocytopenia can be classified into three main categories based on its underlying cause:

1. Immune thrombocytopenia (ITP): An autoimmune disorder where the immune system mistakenly attacks and destroys its own platelets, leading to a decreased platelet count. ITP can be further divided into primary or secondary forms, depending on whether it occurs alone or as a result of another medical condition or medication.
2. Decreased production: Thrombocytopenia can occur when there is insufficient production of platelets in the bone marrow due to various causes, such as viral infections, chemotherapy, radiation therapy, leukemia, aplastic anemia, or vitamin B12 or folate deficiency.
3. Increased destruction or consumption: Thrombocytopenia can also result from increased platelet destruction or consumption due to conditions like disseminated intravascular coagulation (DIC), thrombotic thrombocytopenic purpura (TTP), hemolytic uremic syndrome (HUS), or severe bacterial infections.

Symptoms of thrombocytopenia may include easy bruising, prolonged bleeding from cuts, spontaneous nosebleeds, bleeding gums, blood in urine or stools, and skin rashes like petechiae (small red or purple spots) or purpura (larger patches). The severity of symptoms can vary depending on the degree of thrombocytopenia and the presence of any underlying conditions. Treatment for thrombocytopenia depends on the cause and may include medications, transfusions, or addressing the underlying condition.

Hydroxyethyl starch derivatives are modified starches that are used as plasma expanders in medicine. They are created by chemically treating corn, potato, or wheat starch with hydroxylethyl groups, which makes the starch more soluble and less likely to be broken down by enzymes in the body. This results in a large molecule that can remain in the bloodstream for an extended period, increasing intravascular volume and improving circulation.

These derivatives are available in different molecular weights and substitution patterns, which affect their pharmacokinetics and pharmacodynamics. They are used to treat or prevent hypovolemia (low blood volume) due to various causes such as bleeding, burns, or dehydration. Common brand names include Hetastarch, Pentastarch, and Voluven.

It's important to note that the use of hydroxyethyl starch derivatives has been associated with adverse effects, including kidney injury, coagulopathy, and pruritus (severe itching). Therefore, their use should be carefully monitored and restricted to specific clinical situations.

Alpha-2-antiplasmin (α2AP) is a protein found in the blood plasma that inhibits fibrinolysis, the process by which blood clots are broken down. It does this by irreversibly binding to and inhibiting plasmin, an enzyme that degrades fibrin clots.

Alpha-2-antiplasmin is one of the most important regulators of fibrinolysis, helping to maintain a balance between clot formation and breakdown. Deficiencies or dysfunction in alpha-2-antiplasmin can lead to an increased risk of bleeding due to uncontrolled plasmin activity.

Early ambulation, also known as early mobilization or early rehabilitation, refers to the practice of encouraging patients to get out of bed and start moving around as soon as possible after a surgical procedure or medical event such as a stroke. The goal of early ambulation is to prevent complications associated with prolonged bed rest, including muscle weakness, joint stiffness, blood clots, pneumonia, and pressure ulcers. It can also help improve patients' overall recovery, strength, and functional ability.

The specific timeline for early ambulation will depend on the individual patient's medical condition and healthcare provider's recommendations. However, in general, it is recommended to start mobilizing patients as soon as they are medically stable and able to do so safely, often within the first 24-48 hours after surgery or an event. This may involve sitting up in bed, standing, taking a few steps with assistance, or walking a short distance with the help of a walker or other assistive device.

Healthcare providers such as physicians, nurses, and physical therapists work together to develop a safe and effective early ambulation plan for each patient, taking into account their individual needs, abilities, and limitations.

In the field of medicine, "time factors" refer to the duration of symptoms or time elapsed since the onset of a medical condition, which can have significant implications for diagnosis and treatment. Understanding time factors is crucial in determining the progression of a disease, evaluating the effectiveness of treatments, and making critical decisions regarding patient care.

For example, in stroke management, "time is brain," meaning that rapid intervention within a specific time frame (usually within 4.5 hours) is essential to administering tissue plasminogen activator (tPA), a clot-busting drug that can minimize brain damage and improve patient outcomes. Similarly, in trauma care, the "golden hour" concept emphasizes the importance of providing definitive care within the first 60 minutes after injury to increase survival rates and reduce morbidity.

Time factors also play a role in monitoring the progression of chronic conditions like diabetes or heart disease, where regular follow-ups and assessments help determine appropriate treatment adjustments and prevent complications. In infectious diseases, time factors are crucial for initiating antibiotic therapy and identifying potential outbreaks to control their spread.

Overall, "time factors" encompass the significance of recognizing and acting promptly in various medical scenarios to optimize patient outcomes and provide effective care.

Endoscopy is a medical procedure that involves the use of an endoscope, which is a flexible tube with a light and camera at the end, to examine the interior of a body cavity or organ. The endoscope is inserted through a natural opening in the body, such as the mouth or anus, or through a small incision. The images captured by the camera are transmitted to a monitor, allowing the physician to visualize the internal structures and detect any abnormalities, such as inflammation, ulcers, or tumors. Endoscopy can also be used for diagnostic purposes, such as taking tissue samples for biopsy, or for therapeutic purposes, such as removing polyps or performing minimally invasive surgeries.

Factor IX is also known as Christmas factor, which is a protein that plays a crucial role in the coagulation cascade, a series of chemical reactions that leads to the formation of a blood clot. It is one of the essential components required for the proper functioning of the body's natural blood-clotting mechanism.

Factor IX is synthesized in the liver and activated when it comes into contact with an injured blood vessel. Once activated, it collaborates with other factors to convert factor X to its active form, which then converts prothrombin to thrombin. Thrombin is responsible for converting fibrinogen to fibrin, forming a stable fibrin clot that helps stop bleeding and promote healing.

Deficiencies in Factor IX can lead to hemophilia B, a genetic disorder characterized by prolonged bleeding and an increased risk of spontaneous bleeding. Hemophilia B is inherited in an X-linked recessive pattern, meaning it primarily affects males, while females serve as carriers of the disease. Treatment for hemophilia B typically involves replacing the missing or deficient Factor IX through infusions to prevent or manage bleeding episodes.

In medical terms, pressure is defined as the force applied per unit area on an object or body surface. It is often measured in millimeters of mercury (mmHg) in clinical settings. For example, blood pressure is the force exerted by circulating blood on the walls of the arteries and is recorded as two numbers: systolic pressure (when the heart beats and pushes blood out) and diastolic pressure (when the heart rests between beats).

Pressure can also refer to the pressure exerted on a wound or incision to help control bleeding, or the pressure inside the skull or spinal canal. High or low pressure in different body systems can indicate various medical conditions and require appropriate treatment.

Purinergic P2Y12 receptors are a type of G protein-coupled receptor that bind to and are activated by adenosine diphosphate (ADP). These receptors play an important role in regulating platelet activation and aggregation, which is crucial for the normal hemostatic response to vascular injury.

The P2Y12 receptor is a key component of the platelet signaling pathway that leads to the activation of integrin αIIbβ3, which mediates platelet aggregation. Inhibition of the P2Y12 receptor with drugs such as clopidogrel or ticagrelor is a standard treatment for preventing thrombosis in patients at risk of arterial occlusion, such as those with acute coronary syndrome or following percutaneous coronary intervention.

P2Y12 receptors are also expressed on other cell types, including immune cells and neurons, where they play roles in inflammation, neurotransmission, and other physiological processes.

Hemodilution is a medical term that refers to the reduction in the concentration of certain components in the blood, usually referring to red blood cells (RBCs) or hemoglobin. This occurs when an individual's plasma volume expands due to the infusion of intravenous fluids or the body's own production of fluid, such as during severe infection or inflammation. As a result, the number of RBCs per unit of blood decreases, leading to a lower hematocrit and hemoglobin level. It is important to note that while hemodilution reduces the concentration of RBCs in the blood, it does not necessarily indicate anemia or blood loss.

Heparin is defined as a highly sulfated glycosaminoglycan (a type of polysaccharide) that is widely present in many tissues, but is most commonly derived from the mucosal tissues of mammalian lungs or intestinal mucosa. It is an anticoagulant that acts as an inhibitor of several enzymes involved in the blood coagulation cascade, primarily by activating antithrombin III which then neutralizes thrombin and other clotting factors.

Heparin is used medically to prevent and treat thromboembolic disorders such as deep vein thrombosis, pulmonary embolism, and certain types of heart attacks. It can also be used during hemodialysis, cardiac bypass surgery, and other medical procedures to prevent the formation of blood clots.

It's important to note that while heparin is a powerful anticoagulant, it does not have any fibrinolytic activity, meaning it cannot dissolve existing blood clots. Instead, it prevents new clots from forming and stops existing clots from growing larger.

Blood platelet disorders are conditions that affect the number and/or function of platelets, which are small blood cells that help your body form clots to stop bleeding. Normal platelet count ranges from 150,000 to 450,000 platelets per microliter of blood. A lower-than-normal platelet count is called thrombocytopenia, while a higher-than-normal platelet count is called thrombocytosis.

There are several types of platelet disorders, including:

1. Immune thrombocytopenia (ITP): A condition in which the immune system mistakenly attacks and destroys platelets, leading to a low platelet count. ITP can be acute (lasting less than six months) or chronic (lasting longer than six months).
2. Thrombotic thrombocytopenic purpura (TTP): A rare but serious condition that causes blood clots to form in small blood vessels throughout the body, leading to a low platelet count, anemia, and other symptoms.
3. Hemolytic uremic syndrome (HUS): A condition that is often caused by a bacterial infection, which can lead to the formation of blood clots in the small blood vessels of the kidneys, resulting in kidney damage and a low platelet count.
4. Hereditary platelet disorders: Some people inherit genetic mutations that can affect the number or function of their platelets, leading to bleeding disorders such as von Willebrand disease or Bernard-Soulier syndrome.
5. Medication-induced thrombocytopenia: Certain medications can cause a decrease in platelet count as a side effect.
6. Platelet dysfunction disorders: Some conditions can affect the ability of platelets to function properly, leading to bleeding disorders such as von Willebrand disease or storage pool deficiency.

Symptoms of platelet disorders may include easy bruising, prolonged bleeding from cuts or injuries, nosebleeds, blood in urine or stools, and in severe cases, internal bleeding. Treatment for platelet disorders depends on the underlying cause and may include medications, surgery, or other therapies.

Thromboembolism is a medical condition that refers to the obstruction of a blood vessel by a thrombus (blood clot) that has formed elsewhere in the body and then been transported by the bloodstream to a narrower vessel, where it becomes lodged. This process can occur in various parts of the body, leading to different types of thromboembolisms:

1. Deep Vein Thrombosis (DVT): A thrombus forms in the deep veins, usually in the legs or pelvis, and then breaks off and travels to the lungs, causing a pulmonary embolism.
2. Pulmonary Embolism (PE): A thrombus formed elsewhere, often in the deep veins of the legs, dislodges and travels to the lungs, blocking one or more pulmonary arteries. This can lead to shortness of breath, chest pain, and potentially life-threatening complications if not treated promptly.
3. Cerebral Embolism: A thrombus formed in another part of the body, such as the heart or carotid artery, dislodges and travels to the brain, causing a stroke or transient ischemic attack (TIA).
4. Arterial Thromboembolism: A thrombus forms in an artery and breaks off, traveling to another part of the body and blocking blood flow to an organ or tissue, leading to potential damage or loss of function. Examples include mesenteric ischemia (intestinal damage due to blocked blood flow) and retinal artery occlusion (vision loss due to blocked blood flow in the eye).

Prevention, early detection, and appropriate treatment are crucial for managing thromboembolism and reducing the risk of severe complications.

Plasminogen Activator Inhibitor 1 (PAI-1) is a protein involved in the regulation of fibrinolysis, which is the body's natural process of breaking down blood clots. PAI-1 inhibits tissue plasminogen activator (tPA) and urokinase-type plasminogen activator (uPA), two enzymes that convert plasminogen to plasmin, which degrades fibrin clots. Therefore, PAI-1 acts as a natural antagonist of the fibrinolytic system, promoting clot formation and stability. Increased levels of PAI-1 have been associated with thrombotic disorders, such as deep vein thrombosis and pulmonary embolism.

Gastroscopy is a medical procedure that involves the insertion of a gastroscope, which is a thin, flexible tube with a camera and light on the end, through the mouth and into the digestive tract. The gastroscope allows the doctor to visually examine the lining of the esophagus, stomach, and duodenum (the first part of the small intestine) for any abnormalities such as inflammation, ulcers, or tumors.

The procedure is usually performed under sedation to minimize discomfort, and it typically takes only a few minutes to complete. Gastroscopy can help diagnose various conditions, including gastroesophageal reflux disease (GERD), gastritis, stomach ulcers, and Barrett's esophagus. It can also be used to take tissue samples for biopsy or to treat certain conditions, such as bleeding or the removal of polyps.

Thrombomodulin is a protein that is found on the surface of endothelial cells, which line the interior surface of blood vessels. It plays an important role in the regulation of blood coagulation (clotting) and the activation of natural anticoagulant pathways. Thrombomodulin binds to thrombin, a protein involved in blood clotting, and changes its function from promoting coagulation to inhibiting it. This interaction also activates protein C, an important anticoagulant protein, which helps to prevent the excessive formation of blood clots. Thrombomodulin also has anti-inflammatory properties and is involved in the maintenance of the integrity of the endothelial cell lining.

Electrosurgery is a surgical procedure that uses high-frequency electrical currents to cut, coagulate, or fulgurate tissue. It is often used in surgical procedures as an alternative to traditional scalpels and electrocautery. The electrical currents are delivered through a specialized instrument called an electrosurgical unit (ESU) that can be set to produce different forms of energy, including cutting, coagulation, or blended currents.

During the procedure, the ESU is used to apply electrical energy to the target tissue, which responds by heating up and vaporizing, allowing for precise cuts to be made. The heat generated during the procedure also helps to seal off blood vessels and nerve endings, reducing bleeding and minimizing post-operative pain.

Electrosurgery is commonly used in a variety of surgical procedures, including dermatology, gynecology, urology, orthopedics, and general surgery. It offers several advantages over traditional surgical techniques, such as reduced blood loss, shorter operating times, and faster recovery times for patients. However, it also requires specialized training and equipment to ensure safe and effective use.

Collagen is the most abundant protein in the human body, and it is a major component of connective tissues such as tendons, ligaments, skin, and bones. Collagen provides structure and strength to these tissues and helps them to withstand stretching and tension. It is made up of long chains of amino acids, primarily glycine, proline, and hydroxyproline, which are arranged in a triple helix structure. There are at least 16 different types of collagen found in the body, each with slightly different structures and functions. Collagen is important for maintaining the integrity and health of tissues throughout the body, and it has been studied for its potential therapeutic uses in various medical conditions.

A blood transfusion is a medical procedure in which blood or its components are transferred from one individual (donor) to another (recipient) through a vein. The donated blood can be fresh whole blood, packed red blood cells, platelets, plasma, or cryoprecipitate, depending on the recipient's needs. Blood transfusions are performed to replace lost blood due to severe bleeding, treat anemia, support patients undergoing major surgeries, or manage various medical conditions such as hemophilia, thalassemia, and leukemia. The donated blood must be carefully cross-matched with the recipient's blood type to minimize the risk of transfusion reactions.

Equipment design, in the medical context, refers to the process of creating and developing medical equipment and devices, such as surgical instruments, diagnostic machines, or assistive technologies. This process involves several stages, including:

1. Identifying user needs and requirements
2. Concept development and brainstorming
3. Prototyping and testing
4. Design for manufacturing and assembly
5. Safety and regulatory compliance
6. Verification and validation
7. Training and support

The goal of equipment design is to create safe, effective, and efficient medical devices that meet the needs of healthcare providers and patients while complying with relevant regulations and standards. The design process typically involves a multidisciplinary team of engineers, clinicians, designers, and researchers who work together to develop innovative solutions that improve patient care and outcomes.

Adenosine diphosphate (ADP) is a chemical compound that plays a crucial role in energy transfer within cells. It is a nucleotide, which consists of a adenosine molecule (a sugar molecule called ribose attached to a nitrogenous base called adenine) and two phosphate groups.

In the cell, ADP functions as an intermediate in the conversion of energy from one form to another. When a high-energy phosphate bond in ADP is broken, energy is released and ADP is converted to adenosine triphosphate (ATP), which serves as the main energy currency of the cell. Conversely, when ATP donates a phosphate group to another molecule, it is converted back to ADP, releasing energy for the cell to use.

ADP also plays a role in blood clotting and other physiological processes. In the coagulation cascade, ADP released from damaged red blood cells can help activate platelets and initiate the formation of a blood clot.

Antifibrinolytic agents are a class of medications that inhibit the breakdown of blood clots. They work by blocking the action of enzymes called plasminogen activators, which convert plasminogen to plasmin, the main enzyme responsible for breaking down fibrin, a protein that forms the framework of a blood clot.

By preventing the conversion of plasminogen to plasmin, antifibrinolytic agents help to stabilize existing blood clots and prevent their premature dissolution. These medications are often used in clinical settings where excessive bleeding is a concern, such as during or after surgery, childbirth, or trauma.

Examples of antifibrinolytic agents include tranexamic acid, aminocaproic acid, and epsilon-aminocaproic acid. While these medications can be effective in reducing bleeding, they also carry the risk of thromboembolic events, such as deep vein thrombosis or pulmonary embolism, due to their pro-coagulant effects. Therefore, they should be used with caution and only under the close supervision of a healthcare provider.

Prospective studies, also known as longitudinal studies, are a type of cohort study in which data is collected forward in time, following a group of individuals who share a common characteristic or exposure over a period of time. The researchers clearly define the study population and exposure of interest at the beginning of the study and follow up with the participants to determine the outcomes that develop over time. This type of study design allows for the investigation of causal relationships between exposures and outcomes, as well as the identification of risk factors and the estimation of disease incidence rates. Prospective studies are particularly useful in epidemiology and medical research when studying diseases with long latency periods or rare outcomes.

Epinephrine, also known as adrenaline, is a hormone and a neurotransmitter that is produced in the body. It is released by the adrenal glands in response to stress or excitement, and it prepares the body for the "fight or flight" response. Epinephrine works by binding to specific receptors in the body, which causes a variety of physiological effects, including increased heart rate and blood pressure, improved muscle strength and alertness, and narrowing of the blood vessels in the skin and intestines. It is also used as a medication to treat various medical conditions, such as anaphylaxis (a severe allergic reaction), cardiac arrest, and low blood pressure.

Gelatin is not strictly a medical term, but it is often used in medical contexts. Medically, gelatin is recognized as a protein-rich substance that is derived from collagen, which is found in the skin, bones, and connective tissue of animals. It is commonly used in the production of various medical and pharmaceutical products such as capsules, wound dressings, and drug delivery systems due to its biocompatibility and ability to form gels.

In a broader sense, gelatin is a translucent, colorless, flavorless food ingredient that is derived from collagen through a process called hydrolysis. It is widely used in the food industry as a gelling agent, thickener, stabilizer, and texturizer in various foods such as candies, desserts, marshmallows, and yogurts.

It's worth noting that while gelatin has many uses, it may not be suitable for vegetarians or those with dietary restrictions since it is derived from animal products.

Therapeutic embolization is a medical procedure that involves intentionally blocking or obstructing blood vessels to stop excessive bleeding or block the flow of blood to a tumor or abnormal tissue. This is typically accomplished by injecting small particles, such as microspheres or coils, into the targeted blood vessel through a catheter, which is inserted into a larger blood vessel and guided to the desired location using imaging techniques like X-ray or CT scanning. The goal of therapeutic embolization is to reduce the size of a tumor, control bleeding, or block off abnormal blood vessels that are causing problems.

Thrombopoiesis is the process of formation and development of thrombocytes or platelets, which are small, colorless cell fragments in our blood that play an essential role in clotting. Thrombopoiesis occurs inside the bone marrow, where stem cells differentiate into megakaryoblasts, then progressively develop into promegakaryocytes and megakaryocytes. These megakaryocytes subsequently undergo a process called cytoplasmic fragmentation to produce platelets.

The regulation of thrombopoiesis is primarily controlled by the hormone thrombopoietin (TPO), which is produced mainly in the liver and binds to the thrombopoietin receptor (c-Mpl) on megakaryocytes and their precursors. This binding stimulates the proliferation, differentiation, and maturation of megakaryocytes, leading to an increase in platelet production.

Abnormalities in thrombopoiesis can result in conditions such as thrombocytopenia (low platelet count) or thrombocytosis (high platelet count), which may be associated with bleeding disorders or increased risk of thrombosis, respectively.

Factor XIII, also known as fibrin stabilizing factor, is a protein involved in the clotting process of blood. It is a transglutaminase enzyme that cross-links fibrin molecules to form a stable clot. Factor XIII becomes activated during the coagulation cascade, and its activity helps strengthen the clot and protect it from premature degradation by proteolytic enzymes. A deficiency in Factor XIII can lead to a bleeding disorder characterized by prolonged bleeding after injury or surgery.

Integrin alpha2, also known as CD49b or ITGA2, is a type I transmembrane glycoprotein that forms a heterodimer with integrin beta1 to create the collagen receptor very late antigen-2 (VLA-2) or α2β1 integrin. This integrin plays crucial roles in various cellular processes such as adhesion, migration, and signaling during embryonic development, hemostasis, and tissue repair. It specifically binds to collagen types I, II, and IV, contributing to the regulation of cell-matrix interactions in several tissues, including bone, cartilage, and vascular systems. Integrin alpha2 also participates in immune responses by mediating lymphocyte adhesion and activation.

Esophageal varices and gastric varices are abnormal, enlarged veins in the lower part of the esophagus (the tube that connects the throat to the stomach) and in the stomach lining, respectively. They occur as a result of increased pressure in the portal vein, which is the large blood vessel that carries blood from the digestive organs to the liver. This condition is known as portal hypertension.

Esophageal varices are more common than gastric varices and tend to be more symptomatic. They can cause bleeding, which can be life-threatening if not treated promptly. Gastric varices may also bleed, but they are often asymptomatic until they rupture.

The most common causes of esophageal and gastric varices are cirrhosis (scarring of the liver) and portal hypertension due to other liver diseases such as schistosomiasis or Budd-Chiari syndrome. Treatment options for esophageal and gastric varices include medications to reduce bleeding, endoscopic therapies to treat active bleeding or prevent recurrent bleeding, and surgical procedures to relieve portal hypertension.

Surgical equipment refers to the specialized tools and instruments used by medical professionals during surgical procedures. These devices are designed to assist in various aspects of surgery, such as cutting, grasping, retraction, clamping, and suturing. Surgical equipment can be categorized into several types based on their function and use:

1. Cutting instruments: These include scalpels, scissors, and surgical blades designed to cut through tissues with precision and minimal trauma.

2. Grasping forceps: Forceps are used to hold, manipulate, or retrieve tissue, organs, or other surgical tools. Examples include Babcock forceps, Kelly forceps, and Allis tissue forceps.

3. Retractors: These devices help to expose deeper structures by holding open body cavities or tissues during surgery. Common retractors include Weitlaner retractors, Army-Navy retractors, and self-retaining retractors like the Bookwalter system.

4. Clamps: Used for occluding blood vessels, controlling bleeding, or approximating tissue edges before suturing. Examples of clamps are hemostats, bulldog clips, and Satinsky clamps.

5. Suction devices: These tools help remove fluids, debris, and smoke from the surgical site, improving visibility for the surgeon. Examples include Yankauer suctions and Frazier tip suctions.

6. Needle holders: Specialized forceps designed to hold suture needles securely during the process of suturing or approximating tissue edges.

7. Surgical staplers: Devices that place linear staple lines in tissues, used for quick and efficient closure of surgical incisions or anastomoses (joining two structures together).

8. Cautery devices: Electrosurgical units that use heat generated by electrical current to cut tissue and coagulate bleeding vessels.

9. Implants and prosthetics: Devices used to replace or reinforce damaged body parts, such as artificial joints, heart valves, or orthopedic implants.

10. Monitoring and navigation equipment: Advanced tools that provide real-time feedback on patient physiology, surgical site anatomy, or instrument positioning during minimally invasive procedures.

These are just a few examples of the diverse range of instruments and devices used in modern surgery. The choice of tools depends on various factors, including the type of procedure, patient characteristics, and surgeon preference.

Thrombin receptors are a type of G protein-coupled receptor (GPCR) that play a crucial role in hemostasis and thrombosis. They are activated by the protease thrombin, which is generated during the coagulation cascade. There are two main types of thrombin receptors: protease-activated receptor 1 (PAR-1) and PAR-4.

PAR-1 is expressed on various cell types including platelets, endothelial cells, and smooth muscle cells, while PAR-4 is primarily expressed on platelets. Activation of these receptors triggers a variety of intracellular signaling pathways that lead to diverse cellular responses such as platelet activation, aggregation, and secretion; vasoconstriction; and inflammation.

Dysregulation of thrombin receptor signaling has been implicated in several pathological conditions, including arterial and venous thrombosis, atherosclerosis, and cancer. Therefore, thrombin receptors are considered important therapeutic targets for the treatment of these disorders.

Sclerotherapy is a medical procedure used to treat varicose veins and spider veins. It involves the injection of a solution (called a sclerosant) directly into the affected vein, which causes the vein to collapse and eventually fade away. The sclerosant works by irritating the lining of the vein, causing it to swell and stick together, which then leads to clotting and the eventual reabsorption of the vein by the body.

The procedure is typically performed in a doctor's office or outpatient setting and may require multiple sessions depending on the severity and number of veins being treated. Common side effects include bruising, swelling, and discomfort at the injection site, as well as the possibility of developing brownish pigmentation or small ulcers near the treatment area. However, these side effects are usually temporary and resolve on their own within a few weeks.

Sclerotherapy is considered a safe and effective treatment for varicose veins and spider veins, with high success rates and low complication rates. It is important to note that while sclerotherapy can improve the appearance of affected veins, it does not prevent new veins from developing in the future.

Factor V, also known as proaccelerin or labile factor, is a protein involved in the coagulation cascade, which is a series of chemical reactions that leads to the formation of a blood clot. Factor V acts as a cofactor for the activation of Factor X to Factor Xa, which is a critical step in the coagulation cascade.

When blood vessels are damaged, the coagulation cascade is initiated to prevent excessive bleeding. During this process, Factor V is activated by thrombin, another protein involved in coagulation, and then forms a complex with activated Factor X and calcium ions on the surface of platelets or other cells. This complex converts prothrombin to thrombin, which then converts fibrinogen to fibrin to form a stable clot.

Deficiency or dysfunction of Factor V can lead to bleeding disorders such as hemophilia B or factor V deficiency, while mutations in the gene encoding Factor V can increase the risk of thrombosis, as seen in the Factor V Leiden mutation.

Gas lasers are a type of laser that uses a gas as the gain medium, or the material through which the laser beam is amplified. In a gas laser, the gas is excited electrically or through the use of a radio frequency (RF) generator, causing the atoms or molecules within the gas to emit light at specific wavelengths.

The most common type of gas laser is the helium-neon (HeNe) laser, which produces a red beam at a wavelength of 632.8 nanometers. Other types of gas lasers include the carbon dioxide (CO2) laser, which produces an infrared beam and is commonly used for industrial cutting and welding applications, and the nitrogen laser, which produces a ultraviolet beam.

Gas lasers are known for their high efficiency, stability, and long lifespan. They are also relatively easy to maintain and operate, making them popular choices for a variety of industrial, scientific, and medical applications. In medicine, gas lasers are used for procedures such as laser surgery, where they can be used to cut or coagulate tissue with high precision.

Uterine hemorrhage, also known as uterine bleeding or gynecological bleeding, is an abnormal loss of blood from the uterus. It can occur in various clinical settings such as menstruation (known as menorrhagia), postpartum period (postpartum hemorrhage), or in non-pregnant women (dysfunctional uterine bleeding). The bleeding may be light to heavy, intermittent or continuous, and can be accompanied by symptoms such as pain, dizziness, or fainting. Uterine hemorrhage is a common gynecological problem that can have various underlying causes, including hormonal imbalances, structural abnormalities, coagulopathies, and malignancies. It is important to seek medical attention if experiencing heavy or prolonged uterine bleeding to determine the cause and receive appropriate treatment.

In biology, hemostasis or haemostasis is a process to prevent and stop bleeding, meaning to keep blood within a damaged blood ... Hemostasis can be achieved by chemical agent as well as mechanical or physical agents. Which hemostasis type used is determined ... When the body is under shock and stress, hemostasis is harder to achieve. Though natural hemostasis is most desired, having ... and give off chemical responses that decrease the time it takes for the hemostasis pathway to start. The body's hemostasis ...
... is the process of controlling the bleeding from bone. Bone is a living vascular organ containing channels for ... The bone wax is smeared across the bleeding edge of the bone, blocking the holes and causing immediate hemostasis. Because of ...
... 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 ...
... : Impact for clinical haemostasis laboratories. Thrombosis and Haemostasis, 95, 362-372 (2006). Attard ... Seminars in Thrombosis and Hemostasis. 37(7):723-9 (2011). Monagle, Ignjatovic V, Savoia H. Haemostasis in neonates and ... Developmental Haemostasis is a term that represents the maturation of the haemostatic system from birth to adulthood. There are ... Journal of Thrombosis and Haemostasis. 10(2)298-300 (2012). Newall F*, Ignjatovic V*, Summerhayes R, Gan A, Butt W, Johnston L ...
"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 ...
It is an official journal of the International Society on Thrombosis and Haemostasis. According to the Journal Citation Reports ... 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 ...
Journal of Thrombosis and Haemostasis, official medical journal of the ISTH Research and Practice in Thrombosis and Haemostasis ... 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 ... It was founded in 1954 as the International Committee on Thrombosis and Haemostasis (ICTH). The society was reorganized in 1969 ...
Hemostasis. 13 (3): 298-306. doi:10.1055/s-2007-1003505. PMID 3317840. Raugi, R.J.; Olerud, J.E.; Gown, A.M. (1987). " ...
Teruel-Montoya R, Rosendaal FR, Martínez C (February 2015). "MicroRNAs in hemostasis". Journal of Thrombosis and Haemostasis. ... Journal of Thrombosis and Haemostasis. 16 (11): 2233-2245. doi:10.1111/jth.14290. PMID 30207063. Nourse J, Danckwardt S ( ...
Kuhl H (May 1996). "Effects of progestogens on haemostasis". Maturitas. 24 (1-2): 1-19. doi:10.1016/0378-5122(96)00994-2. PMID ... effects on hemostasis". Expert Rev Clin Pharmacol. 10 (10): 1129-1144. doi:10.1080/17512433.2017.1356718. PMID 28712325. S2CID ...
"Classic and Global Hemostasis Testing in Pregnancy and during Pregnancy Complications". Seminars in Thrombosis and Hemostasis. ... O'Riordan, Máiread N; Higgins, John R (June 2003). "Haemostasis in normal and abnormal pregnancy". Best Practice & Research ... Hellgren M (April 2003). "Hemostasis during normal pregnancy and puerperium". Semin Thromb Hemost. 29 (2): 125-30. doi:10.1055/ ... Canonico M (July 2014). "Hormone therapy and hemostasis among postmenopausal women: a review" (PDF). Menopause. 21 (7): 753-62 ...
Kuhl H (May 1996). "Effects of progestogens on haemostasis". Maturitas. 24 (1-2): 1-19. doi:10.1016/0378-5122(96)00994-2. PMID ... Barco S, Nijkeuter M, Middeldorp S (July 2013). "Pregnancy and venous thromboembolism". Seminars in Thrombosis and Hemostasis. ... Schindler AE (December 2003). "Differential effects of progestins on hemostasis". Maturitas. 46 (Suppl 1): S31-7. doi:10.1016/j ... Skouby SO, Sidelmann JJ (November 2018). "Impact of progestogens on hemostasis". Hormone Molecular Biology and Clinical ...
Hemostasis in Cardiac. Blackwell Publishing. pp. 118-120. ISBN 9780879934101. Oleg V. Kim; Rustem I. Litvinov; Mark S. Alber; ...
Jackson, Karen V. (2021). "Immunohematology and hemostasis". In Walton, Raquel M.; Cowell, Rick L.; Valenciano, Amy C. (eds.). ...
Daughety, Molly M.; Samuelson Bannow, Bethany T. (2019). "Hemostasis and Thrombosis in Pregnancy". Hemostasis and Thrombosis. ...
Fritsma, George A. (2002). "Evaluation of Hemostasis." Hematology: Clinical Principles and Applications . Ed. Bernadette Rodak ... Thrombosis and Haemostasis. 49 (3): 238-44. doi:10.1055/s-0038-1657371. PMID 6879511. S2CID 32051201. Anonymous (1983). "33: ... Journal of Thrombosis and Haemostasis. 18 (5): 1023-1026. doi:10.1111/jth.14810. PMC 9906133. PMID 32338827. Houdijk, W. P.; ... Journal of Thrombosis and Haemostasis. 2 (2): 266-70. doi:10.1111/j.1538-7836.2004.00434.x. PMID 14995988. S2CID 20151897. ...
Manon‐Jensen, T.; Kjeld, N. G.; Karsdal, M. A. (2016). "Collagen-mediated hemostasis". Journal of Thrombosis and Haemostasis. ... Manon‐Jensen, T.; Kjeld, N. G.; Karsdal, M. A. (2016). "Collagen-mediated hemostasis". Journal of Thrombosis and Haemostasis. ...
... effects on hemostasis". Expert Review of Clinical Pharmacology. 10 (10): 1129-1144. doi:10.1080/17512433.2017.1356718. PMID ...
Antovic A (October 2010). "The overall hemostasis potential: a laboratory tool for the investigation of global hemostasis". ... Antovic A (July 2008). "Screening haemostasis--looking for global assays: the Overall Haemostasis Potential (OHP) method--a ... He S, Antovic A, Blombäck M (September 2001). "A simple and rapid laboratory method for determination of haemostasis potential ... Curnow J (2017). "The Overall Hemostatic Potential (OHP) Assay". Hemostasis and Thrombosis. Methods Mol Biol. Vol. 1646. pp. ...
... effects on hemostasis". Expert Rev Clin Pharmacol. 10 (10): 1129-1144. doi:10.1080/17512433.2017.1356718. PMID 28712325. S2CID ...
December 2020). "Evaluation of the effect of a new oral contraceptive containing estetrol and drospirenone on hemostasis ... effects on hemostasis". Expert Review of Clinical Pharmacology. 10 (10): 1129-1144. doi:10.1080/17512433.2017.1356718. PMID ...
... effects on hemostasis". Expert Review of Clinical Pharmacology. 10 (10): 1129-1144. doi:10.1080/17512433.2017.1356718. PMID ... Journal of Thrombosis and Haemostasis. 11 (1): 124-131. doi:10.1111/jth.12060. PMID 23136837. S2CID 22306721. Gialeraki A, ... Journal of Thrombosis and Haemostasis. 17 (11): 1790-1797. doi:10.1111/jth.14626. PMID 31465627. S2CID 201673648. Stuenkel CA, ... Clinical and Applied Thrombosis/Hemostasis. 24 (2): 217-225. doi:10.1177/1076029616683802. PMC 6714678. PMID 28049361. Scarabin ...
Kluft C, Lansink M (July 1997). "Effect of oral contraceptives on haemostasis variables". Thromb Haemost. 78 (1): 315-26. doi: ... Hellgren M (April 2003). "Hemostasis during normal pregnancy and puerperium". Semin Thromb Hemost. 29 (2): 125-30. doi:10.1055/ ... effects on hemostasis". Expert Rev Clin Pharmacol. 10 (10): 1129-1144. doi:10.1080/17512433.2017.1356718. PMID 28712325. S2CID ... "A comparison between effects of estradiol valerate and low dose ethinyl estradiol on haemostasis parameters". Thromb Haemost. ...
Hoffman M, Monroe DM (June 2001). "A cell-based model of hemostasis". Thrombosis and Haemostasis. 85 (6): 958-965. doi:10.1055/ ... Platelets immediately form a plug at the site of injury; this is called primary hemostasis. Secondary hemostasis occurs ... forming a platelet plug and thereby completing primary hemostasis). The coagulation cascade of secondary hemostasis has two ... 2009). Practical Hemostasis and Thrombosis. Wiley-Blackwell. p. 2. ISBN 978-1-4051-8460-1. Watson, M. S.; Pallister, C. J. ( ...
Haemostasis 1996;26 Suppl 1:124-30. Hedner U. History of rFVIIa therapy. Thromb Res 2010;125 Suppl 1:S4-6. Key NS, Aledort LM, ... Hemostasis & Thrombosis Research Society ::". Htrs.org. Retrieved 2013-09-05. (Articles with short description, Short ... Lusher served as the Marion I. Barnhart Hemostasis Research Professor and Distinguished Professor of Pediatrics at Wayne State ... and the Hemostasis & Thrombosis Research Society, Lifetime Achievement Award in 2009. "Jeanne Marie Lusher M.D. Obituary - ...
Kitchens, Craig S.; Konkle, Barbara A.; Kessler, Craig M. (2013-02-20). Consultative Hemostasis and Thrombosis. Elsevier Health ... Journal of Thrombosis and Haemostasis. 7: 84-87. doi:10.1111/j.1538-7836.2009.03395.x. ISSN 1538-7836. PMID 19630775. S2CID ...
Hemostasis (blood clotting): Within the first few minutes of injury, platelets in the blood begin to stick to the injured site ... Rasche H (2001). "Haemostasis and thrombosis: an overview". European Heart Journal Supplements. 3 (Supplement Q): Q3-Q7. doi: ... This process is divided into predictable phases: blood clotting (hemostasis), inflammation, tissue growth (cell proliferation ... Wound healing is classically divided into hemostasis, inflammation, proliferation, and remodeling. Although a useful construct ...
Hemostasis involves several components. The main components of the hemostatic system include platelets and the coagulation ... hemostasis and related articles. The discussion here is limited to the common practical aspects of blood clot formation which ... The stopping or controlling of bleeding is called hemostasis and is an important part of both first aid and surgery. Upper head ... The underlying scientific basis for blood clotting and hemostasis is discussed in detail in the articles, coagulation, ...
Wu Q (Feb 2001). "Gene targeting in hemostasis. Hepsin". Frontiers in Bioscience. 6 (3): D192-200. doi:10.2741/a604. PMID ...
2011). Toxins and Hemostasis. Springer 2011. p. 99. ISBN 978-90-481-9294-6. Fox, William Sherwood (1988). The Bruce beckons: ...
In biology, hemostasis or haemostasis is a process to prevent and stop bleeding, meaning to keep blood within a damaged blood ... Hemostasis can be achieved by chemical agent as well as mechanical or physical agents. Which hemostasis type used is determined ... When the body is under shock and stress, hemostasis is harder to achieve. Though natural hemostasis is most desired, having ... and give off chemical responses that decrease the time it takes for the hemostasis pathway to start. The bodys hemostasis ...
Hemostasis : Blood clotting - Download as a PDF or view online for free ... Hemostasis and coagulation of blood For M.Sc & Basic Medical Students by Pand.... Pandian M•2.1K. views ... haemostasis-the rapid arrest of blood loss upon vascular damage, in order to maintain a relatively constant blood volume. • The ... Hemostasis and blood coagulation general pathologySiganga Siganga. 3.7K. views•15. slides ...
Catheter Hemostasis Valve For use with .038" (.096 cm) dia. and smaller guide wires; Product Code: AI-07000. ...
Check-Flo Hemostasis Assembly, Individual product is packaged in a Tyvek-film sterilizable outer pouch.. ...
Hemostasis. Hemostasis starts within the very first moments of the injury, where platelets play a role by aggregating, as well ... While platelets play a crucial role in clot formation during hemostasis, inflammatory cells débride injured tissue during the ... Healing is a systematic process, traditionally explained in terms of 4 overlapping classic phases: hemostasis, inflammation, ...
Hemostasis Analyzer. Semi Automated Hemostasis Instrument. Compact 2-channel instrument device dedicated for small laboratories ...
Manual Hemostasis. Initial treatment begins with direct pressure. The nostrils are squeezed together for 5-30 minutes straight ... may be placed in the affected nostril to help vasoconstrict and achieve hemostasis. ...
Hemostasis Reagents. D-Dimer. D-Dimers is degradation products of fibrin, biomarker for activation of plasma coagulation and/or ...
6 Haematology, Sydney Centres for Thrombosis and Haemostasis, Westmead Hospital, Institute of Clinical Pathology and Medical ... a report of thromboelastography findings and other parameters of hemostasis. J Thromb Haemost 18 (07) 1738-1742 ...
... prospective and randomized controlled trials in diagnosis and endoscopic hemostasis of gastrointestinal (GI) hemorrhage; ... standard endoscopic hemostasis for severe ulcer and Dieulafoys lesion hemorrhage. *Multicenter study of Doppler assisted ... Randomized Controlled Trial (RCT) of a large over-the-scope hemoclip compared to standard endoscopic hemostasis for patients ... RCT of Doppler assisted risk stratification and hemostasis compared to GI guideline management to prevent severe delayed post- ...
Seminars in Thrombosis and Hemostasis LinksSchließen Referenz. Johnston I, Sarkar A, Hayes V. et al. Recognition of PF4-VWF ...
VIII and Factor IX of the Scientific and Standardization Committee of the International Society on Thrombosis and Haemostasis ...
Invited faculty are the worlds foremost basic scientists and clinicians working in the field of hemostasis and thrombosis. ... UNCs 10th Symposium on Hemostasis will take place on April 23-25, 2020 in Chapel Hill, North Carolina. ... The 11th Symposium on Hemostasis is endorsed by the International Society on Thrombosis and Haemostasis. ... 11th Symposium on Hemostasis: Coagulation, Platelet Biology at the Intersection of Health and Disease. April 25-27, 2024 ...
​Kensey KR. Puncture site hemostasis. J Invasive Cardiol. 1994;6(8):273-6
We sought to investigate the efficacy and safety of manual hemostasis in the axillary artery. ,i,Methods,/i,. Data were ... Manual compression was used to achieve the hemostasis of the axillary artery. Vascular and bleeding complications attributable ... Manual compression of the axillary artery appears to be an effective and safe method for achieving hemostasis. Large ... to manual hemostasis were classified based on the Valve Academic Research Consortium-2 (VARC-2) and Bleeding Academic Research ...
Collection, Transport, and Processing of Blood Specimens for Testing Plasma-Based Coagulation Assays and Molecular Hemostasis ...
Explore the mechanisms of hemostasis and matrix degradation. Read now! ... De- cidual cells promote hemostasis through enhanced expression of tissue factor (TF), the primary initiator of hemostasis via ... Thrombosis and Haemostasis, 91, 290-295. [38] Lykke, J.A., Paidas, M.J. and Langhoff-Roos, J. (2009) Recurring complications in ... Mackman, N., Tilley, R.E. and Key, N.S. (2007) Role of the extrinsic pathway of blood coagulation in hemostasis and thrombosis ...
... six achieved excellent hemostasis and one achieved good hemostasis. One had poor hemostasis, and one was unevaluable. ... Hemostasis documented in all but one patient. Adjudicated hemostasis was achieved in 100% of the 113 urgent surgical patients ... "Rates of effective hemostasis were adjudicated as good or excellent in more than 90% of cases with no drug-related serious ... there were 113 surgical cases and 9 major bleeding patients evaluable for hemostasis. ...
... The IHBT Outpatient Department comprises the Centre for Thrombosis and Hemostasis ...
... the hemostasis tests market in Japan was valued at 17.50 in 2022 ... The hemostasis tests market in Japan can expand or contract due ... In the Hemostasis tests market, POC tests often include devices used in physicians offices and for at-home monitoring. ... Hemostasis tests help screen and identify patients with hemostatic defects. GlobalData uses proprietary data and analytics to ... Hemostasis tests includes the sub-segments Prothrombin time tests, Prothrombin time (PT) POC test, Prothrombin time laboratory ...
... Clin Sci (Lond). 1991 Oct;81(4 ... Enteric coating reduced endoscopic signs of injury, but did not affect the impaired haemostasis caused by aspirin.(ABSTRACT ...
Chronic Obstructive Bronchitis and Haemostasis Group Thromb Haemost. 1994 Sep;72(3):343-6. ...
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Pathophysiology of Haemostasis and Thrombosis 1 April 2001; 30 (6): 298-307. https://doi.org/10.1159/000054147 ...
Pathophysiology of Haemostasis and Thrombosis 1 May 1992; 22 (5): 233-235. https://doi.org/10.1159/000216328 ...
Hemostasis: is a process which causes bleeding to stop, meaning to keep blood within a damaged blood vessel. It is the first ... Hemostasis Hemostasis: is a process which causes bleeding to stop, meaning to keep blood within a damaged blood vessel. It is ... Hemostasis has three major steps: 1) vasoconstriction, 2) temporary blockage of a break by a platelet plug, and 3) blood ... Stago EdVantage Virtual University is an educational platform that demystifies hemostasis testing with on-demand webinars and a ...
We provide secure, cost-effective access to the UKs richest collection of digital content: giving you access to the latest data and content from leading international publishers and providers.. Find out more at jisc.ac.uk. ...
This project will study blood cell adhesion and thrombus formation in microfluidic devices to assess for persisting thrombotic tendency in patients with a history of venous clots, who have completed treatment.
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  • When endothelium of a blood vessel is damaged, the endothelial cells stop secretion of coagulation and aggregation inhibitors and instead secrete von Willebrand factor, which initiate the maintenance of hemostasis after injury. (wikipedia.org)
  • Hemostasis involves three major steps: vasoconstriction temporary blockage of a hole in a damaged blood vessel by a platelet plug blood coagulation (formation of fibrin clots) These processes seal the injury or hole until tissues are healed. (wikipedia.org)
  • Hemostasis and coagulation of blood For M.Sc & Basic Medical Students by Pand. (slideshare.net)
  • Mackman, N., Tilley, R.E. and Key, N.S. (2007) Role of the extrinsic pathway of blood coagulation in hemostasis and thrombosis. (scirp.org)
  • Hemostasis has three major steps: 1) vasoconstriction, 2) temporary blockage of a break by a platelet plug, and 3) blood coagulation, or formation of a fibrin clot. (labroots.com)
  • Hemostasis testing can identify patients with blood defects that might result in excessive bleeding, and typically cover three phases of the blood's clotting and wound healing process: coagulation, platelet plug formation and fibrinolysis (the breakdown of clots). (xtalks.com)
  • Gene ontology enrichment analysis revealed alterations in hemostasis/coagulation, metabolism, immune responses, and angiogenesis in PACS vs. healthy controls. (lu.se)
  • The global hemostasis/coagulation analyzer market is estimated to surpass $5,601.5 million by 2027, exhibiting a CAGR of 4.7% from 2020 to 2027. (researchdive.com)
  • The report offers meticulous analysis of the global hemostasis/coagulation analyzer market by thoroughly studying different assets of the market including major segments, market dynamics, regional market conditions, investment opportunities, and top players functioning in the market. (researchdive.com)
  • The report offers market size and forecast by keenly evaluating every segment of the global hemostasis/coagulation analyzer market. (researchdive.com)
  • The report divides the global hemostasis/coagulation analyzer market into four main regions including Europe, North America, Asia-Pacific, and LAMEA. (researchdive.com)
  • Furthermore, these regions are sub-divided to profile detailed panorama of the hemostasis/coagulation analyzer market across major countries in specific regions. (researchdive.com)
  • Apart from these insights, the highlights of major players functioning in the global hemostasis/coagulation analyzer market is also covered in the report. (researchdive.com)
  • A detailed overview of 10 leading players operating in the global hemostasis/coagulation analyzer market is provided to understand their status and hold over the market share. (researchdive.com)
  • Company profile of each player includes several data points such as short overview of the company, major company executives, company's financial status and revenue, major business strategies implemented by company, innovative developments or initiatives taken by company to shove their position and standout among other competitors in the global hemostasis/coagulation analyzer market. (researchdive.com)
  • The research report is formed by collating different statistics and information concerning the hemostasis/coagulation analyzer market. (researchdive.com)
  • Join renowned speakers in five sessions to gain insights into the latest developments in hemostasis testing and the management of coagulation disorders. (siemens-healthineers.com)
  • Human blood coagulation, haemostasis and thrombosis / edited by Rosemary Biggs and C. R. Rizza. (who.int)
  • This negative surface provides binding sites for enzymes and cofactors of the coagulation system, resulting in the formation of a clot (secondary hemostasis). (medscape.com)
  • Platelet disorders lead to defects in primary hemostasis and produce signs and symptoms different from coagulation factor deficiencies (disorders of secondary hemostasis). (medscape.com)
  • Platelet plug formation: Platelets adhere to damaged endothelium to form a platelet plug (primary hemostasis) and then degranulate. (wikipedia.org)
  • While platelets play a crucial role in clot formation during hemostasis, inflammatory cells débride injured tissue during the inflammatory phase. (medscape.com)
  • Hemostasis starts within the very first moments of the injury, where platelets play a role by aggregating, as well as by releasing cytokines, chemokines, and hormones. (medscape.com)
  • Platelets provide the initial hemostasis response. (reportsanddata.com)
  • The initial hemostatic plug, composed primarily of platelets, is stabilized further by a fibrin mesh generated in secondary hemostasis. (medscape.com)
  • We sought to investigate the efficacy and safety of manual hemostasis in the axillary artery. (hindawi.com)
  • Vascular and bleeding complications attributable to manual hemostasis were classified based on the Valve Academic Research Consortium-2 (VARC-2) and Bleeding Academic Research Consortium-2 (BARC-2) classifications, respectively. (hindawi.com)
  • The efficacy of manual hemostasis for axillary vascular access is unknown. (hindawi.com)
  • Therefore, we sought to investigate the use and outcomes of manual hemostasis in the axillary artery for the removal of percutaneously inserted intra-aortic balloon pumps (IABPs). (hindawi.com)
  • However, safe axillary vascular access with effective hemostasis requires special techniques which have not been well described in the literature. (hindawi.com)
  • Rates of effective hemostasis were adjudicated as good or excellent in more than 90% of cases with no drug-related serious adverse events or allergic or infusion-related reactions," reported Deepak L. Bhatt, MD, at the American Heart Association scientific sessions. (the-hospitalist.org)
  • Pathophysiology of Haemostasis and Thrombosis (2001) 30 (6): 298-307. (karger.com)
  • Pathophysiology of Haemostasis and Thrombosis (1992) 22 (5): 233-235. (karger.com)
  • Join this session to learn about the impact of COVID-19 on hemostasis and the pathophysiology of associated coagulopathy. (siemens-healthineers.com)
  • The Hemostasis & Thrombosis Center at University Hospitals Rainbow Babies & Children's Hospital's Angie Fowler Adolescent & Young Adult Cancer Institute and UH Seidman Cancer Center specializes in the care of children with congenital thrombotic disorders, bleeding disorders such as von Willebrand disease and hemophilia , and other rare conditions that increase risk for bleeding or thrombosis . (uhhospitals.org)
  • The Maternal and Child Health Bureau (MCHB) has recognized the Hemostasis & Thrombosis Center as a regional comprehensive treatment center. (uhhospitals.org)
  • Many important educational services are provided at the Hemostasis & Thrombosis Center at UH Rainbow Babies & Children's Hospital. (uhhospitals.org)
  • Jensen DM, Ohning GV, Kovacs TOG, Ghassemi K, Jutabha R, Dulai GS, Machicado GA. Doppler Endoscopic probe as a guide to risk stratification and definitive hemostasis of peptic ulcer bleeding . (uclahealth.org)
  • Enteric coating reduced endoscopic signs of injury, but did not affect the impaired haemostasis caused by aspirin. (nih.gov)
  • Novel simulator of endoscopic hemostasis with actual endoscope and devices. (bvsalud.org)
  • Video 1Demonstration of novel simulator of endoscopic hemostasis . (bvsalud.org)
  • The Quantra Hemostasis System uses proprietary SEER sonorheometry , a medical-grade ultrasound technology, to measure clot stiffness of whole blood samples over time with ultrasound-induced resonance. (xtalks.com)
  • Hemostasis is maintained in the body via three mechanisms: Vascular spasm: Vasoconstriction is produced by vascular smooth muscle cells, and is the blood vessel's first response to injury. (wikipedia.org)
  • Coughlin, S.R. (2005) Protease-activated receptors in hemostasis, thrombosis and vascular biology. (scirp.org)
  • Collagens mediate essential hemostasis by maintaining the integrity and stability of the vascular wall. (nordicbioscience.com)
  • Equipped with a clear polycarbonate housing, female luer lock side port and rotating male luer lock with a blue silicone O-ring, this hemostasis valve accommodates 0 - 9 FR guidewires and is ideal for maintaining hemostasis during the introduction/withdrawl and use of diagnostic and internvetional devices. (qosina.com)
  • Hemostasis Valve Y Connector, Male Luer Slip, Female Luer Lock Sid. (qosina.com)
  • Double Hemostasis Valve Y Connector, Rotating Male Luer Lock, Fema. (qosina.com)
  • By bonding a PVC tube (T4306) into the female luer lock sidearm of a hemostasis valve (80328), you can add a 4-way stopcock (99680) to the other end of the tube, creating a 4-way stopcock sideport. (qosina.com)
  • In biology, hemostasis or haemostasis is a process to prevent and stop bleeding, meaning to keep blood within a damaged blood vessel (the opposite of hemostasis is hemorrhage). (wikipedia.org)
  • Fatal arterial hemorrhage after pancreaticoduodenectomy: How do we simultaneously accomplish complete hemostasis and hepatic arterial flow? (wjgnet.com)
  • Healing is a systematic process, traditionally explained in terms of 4 overlapping classic phases: hemostasis, inflammation, proliferation, and maturation. (medscape.com)
  • This enhances our understanding and might pave the way for future experimental and clinical investigations to elucidate and/or target resolution of inflammation and micro-clots and restore the hemostasis and immunity in PACS. (lu.se)
  • The Royal College of Pathologists of Australasia Quality Assurance Programs (RCPAQAP) will be holding a Haemostasis and Thrombosis Workshop on Friday 5th of July 2019, the day prior to the ISTH Congress, at the Melbourne Convention Centre. (rcpaqap.com.au)
  • The interdisciplinary Center for Blood Oxygen Transport & Hemostasis (CBOTH) addresses fundamental, challenging questions related to blood O 2 transport and hemostasis from a systems perspective, with attention to human biology, physiology and therapeutics. (umaryland.edu)
  • Hemostasis devices and sealants are used to prevent blood loss in various conditions. (express-press-release.net)
  • Additionally, hemostasis and tissue sealants also help in the healing of the damage. (reportsanddata.com)
  • The global hemostasis & tissue sealing agents market size was valued at USD 6.13 billion in 2021 and is anticipated to expand at a compound annual growth rate (CAGR) of 8.8% during the forecast period. (express-press-release.net)
  • The hemostasis and tissue sealing agents market cater to conditions ranging from mild injuries to burns and neurosurgical management. (express-press-release.net)
  • Rising number of surgical processes coupled with increasing trauma cases, increase in road accidents and need for reduction of blood loss coupled with rapid development and launch of innovative tissue sealing compounds are key factors contributing to high CAGR of Hemostasis and Tissue Sealing Agents during forecast period. (reportsanddata.com)
  • Hemostasis and tissue sealing agents are used in medical applications and act as a catalyst in blood clotting. (reportsanddata.com)
  • Hemostasis and Tissue Sealing Agents market is growing at a CAGR of 9% in Asia Pacific followed by North America and Europe, with 8.1 % and 8.0 % CAGR, respectively. (reportsanddata.com)
  • In 2018, Topical Hemostats segment is expected to dominate Hemostasis and Tissue Sealing Agents which holds 51.3% of the global market. (reportsanddata.com)
  • Qosina part #33057 is an ISO 80369-7 compliant, one-handed hemostasis valve y connector. (qosina.com)
  • With a stainless steel spring for one-handed functionality, this hemostasis valve is one of Qosina's large selection of hemostasis valves and stopcocks for all your component needs. (qosina.com)
  • After some exclusions for lack of urgency and reclassifications following adjudication, there were 113 surgical cases and 9 major bleeding patients evaluable for hemostasis. (the-hospitalist.org)
  • Adjudicated hemostasis was achieved in 100% of the 113 urgent surgical patients evaluated. (the-hospitalist.org)
  • In the nine major bleeding patients, six achieved excellent hemostasis and one achieved good hemostasis. (the-hospitalist.org)
  • Hemostasis tests help screen and identify patients with hemostatic defects. (medicaldevice-network.com)
  • The hemostasis system can help clinicians determine which blood products are required to treat specific patients. (xtalks.com)
  • The market grew with the increasing importance of unbalanced hemostasis in COVID-19 patients in favor of a prothrombotic state. (express-press-release.net)
  • In March 2020, the International Society for Thrombosis and Hemostasis launched interim guidelines for the management and recognition of coagulopathy among COVID-19 patients on the basis of ISTH DIC score. (express-press-release.net)
  • Some of the critical factors responsible for propelling the growth of the Hemostasis and tissue sealing market include increasing need to stop the blood during surgical processes, reduction in blood loss, increased demand for surgeries owing to an increase in chronic disease patients, and an increasing number of road accidents. (reportsanddata.com)
  • To enhance haemostasis, SurgicelTM (oxidized cel- lulose) gauze was sometimes used in the tooth socket in patients who were operated under general anaesthesia. (who.int)
  • This is referred to as primary hemostasis. (wikipedia.org)
  • De- cidual cells promote hemostasis through enhanced expression of tissue factor (TF), the primary initiator of hemostasis via thrombin generation, and plasminogen activator inhibitor-1, which inactivates tissue type plasminogen activator, the primary fibrinolytic agent. (scirp.org)
  • When endothelial continuity is disrupted and the underlying matrix is exposed, a coordinated series of events are set in motion to seal the defect (primary hemostasis). (medscape.com)
  • The IHBT Outpatient Department comprises the Centre for Thrombosis and Hemostasis specialized in diagnostics and therapy of blood clotting disorders. (uhkt.cz)
  • This application claims the benefit of U.S. Provisional Application No. 62/616,751, filed Jan. 12, 2018, entitled "Powder for Achieving Hemostasis," the disclosure of which is hereby corporate by reference in its entirety. (justia.com)
  • Leveraging Atellica® Diagnostics IT and lab automation solutions, we help simplify your lab operations beyond hemostasis testing. (siemens-healthineers.com)
  • HemoSonics is a medical device company that develops personalized diagnostic solutions for patient blood management (PBM), and the addition of the QStat Cartridge to their existing Hemostasis System enables it to cover the broadest range of clinical indications in the US. (xtalks.com)
  • Hemostasis Science Weeks is a free, online scientific series that helps connect lab and clinical experts around the world. (siemens-healthineers.com)
  • In this forum, leading independent hemostasis experts share scientific insights into current clinical practice, what's new, and what's coming in hemostasis testing. (siemens-healthineers.com)
  • Wounds, surgical sites, diseased tissue, ulcer beds and gastric varices, among others, are locations where conventional means of hemostasis ray to fail, leading to extended hospital stay or death. (justia.com)
  • Hemostasis occurs when blood is present outside of the body or blood vessels. (wikipedia.org)
  • Hemostasis: is a process which causes bleeding to stop, meaning to keep blood within a damaged blood vessel. (labroots.com)
  • HemoSonics received FDA 510(k) clearance for their point-of-care and laboratory-based whole blood hemostasis testing device. (xtalks.com)
  • The Quantra Hemostasis System with QStat Cartridge is ground-breaking in the field of point-of-care and laboratory-based whole blood hemostasis testing, and the recent clearance expands its indications to now include trauma and liver transplant procedures. (xtalks.com)
  • Von Willebrand factor, integrins and glycoprotein VI, as well as clotting factors, can bind collagen to restore normal hemostasis after trauma. (nordicbioscience.com)
  • Siemens Healthineers and Sysmex hemostasis systems streamline testing and allow standardized results across low-, mid-, and high-volume analyzers for multisite labs. (siemens-healthineers.com)
  • It is anticipated to drive the market growth positively for hemostasis and tissue sealing products in the market during the forecast period. (reportsanddata.com)
  • Minimally invasive surgery is making use of hemostasis and tissue sealing products for urological treatments, thereby promoting the growth of Hemostasis and tissue sealing market. (reportsanddata.com)
  • Compact 2-channel instrument device dedicated for small laboratories to perform hemostasis screening and DDimers tests. (horiba.com)
  • The symposium planned for 2024 will continue to focus on the latest findings in the field of hemostasis and thrombosis. (unc.edu)
  • Journal of Thrombosis and Haemostasis, 3, 1800-1814. (scirp.org)
  • Use the following template to cite a book using the Journal of Thrombosis and Haemostasis citation style. (citethisforme.com)
  • GlobalData uses proprietary data and analytics to provide a comprehensive report on the hemostasis tests market in Japan. (medicaldevice-network.com)
  • Check-Flo Hemostasis Assembly, Individual product is packaged in a Tyvek-film sterilizable outer pouch. (fda.gov)
  • If hemostasis plays a role in your healthcare specialty, these webinars will deliver valuable information and insights for your daily practice. (siemens-healthineers.com)
  • As a leader in hemostasis testing, Siemens Healthineers passionately supports hemostasis research and sharing of scientific insights to make them accessible to experts around the world. (siemens-healthineers.com)
  • Oxygen (O 2 ) transport and hemostasis are central to human adaptation to stress/injury and to disease pathobiology. (umaryland.edu)
  • The 11th Symposium on Hemostasis is endorsed by the International Society on Thrombosis and Haemostasis . (unc.edu)
  • by International Society on Thrombosis and Haemostasis. (who.int)