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.
The process of the interaction of BLOOD COAGULATION FACTORS that results in an insoluble FIBRIN clot.
Laboratory tests for evaluating the individual's clotting mechanism.
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.
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.
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.
Endogenous substances, usually proteins, that are involved in the blood coagulation process.
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.
Hemorrhagic necrosis that was first demonstrated in rabbits with a two-step reaction, an initial local (intradermal) or general (intravenous) injection of a priming endotoxin (ENDOTOXINS) followed by a second intravenous endotoxin injection (provoking agent) 24 h later. The acute inflammation damages the small blood vessels. The following intravascular coagulation leads to capillary and venous THROMBOSIS and NECROSIS. Shwartzman phenomenon can also occur in other species with a single injection of a provoking agent, and during infections or pregnancy. Its susceptibility depends on the status of IMMUNE SYSTEM, coagulation, FIBRINOLYSIS, and blood flow.
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.
Blocking of maternal circulation by AMNIOTIC FLUID that is forced into uterine VEINS by strong UTERINE CONTRACTION near the end of pregnancy. It is characterized by the sudden onset of severe respiratory distress and HYPOTENSION that can lead to maternal DEATH.
A protein derived from FIBRINOGEN in the presence of THROMBIN, which forms part of the blood clot.
A serine proteinase inhibitor used therapeutically in the treatment of pancreatitis, disseminated intravascular coagulation (DIC), and as a regional anticoagulant for hemodialysis. The drug inhibits the hydrolytic effects of thrombin, plasmin, and kallikrein, but not of chymotrypsin and aprotinin.
The natural enzymatic dissolution of FIBRIN.
Death of cells in the KIDNEY CORTEX, a common final result of various renal injuries including HYPOXIA; ISCHEMIA; and drug toxicity.
The number of PLATELETS per unit volume in a sample of venous BLOOD.
The use of ultrasound to guide minimally invasive surgical procedures such as needle ASPIRATION BIOPSY; DRAINAGE; etc. Its widest application is intravascular ultrasound imaging but it is useful also in urology and intra-abdominal conditions.
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.
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.
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.
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).
Systemic inflammatory response syndrome with a proven or suspected infectious etiology. When sepsis is associated with organ dysfunction distant from the site of infection, it is called severe sepsis. When sepsis is accompanied by HYPOTENSION despite adequate fluid infusion, it is called SEPTIC SHOCK.
The number of LEUKOCYTES and ERYTHROCYTES per unit volume in a sample of venous BLOOD. A complete blood count (CBC) also includes measurement of the HEMOGLOBIN; HEMATOCRIT; and ERYTHROCYTE INDICES.
Death resulting from the presence of a disease in an individual, as shown by a single case report or a limited number of patients. This should be differentiated from DEATH, the physiological cessation of life and from MORTALITY, an epidemiological or statistical concept.
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.
A subnormal level of BLOOD PLATELETS.
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.
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.
Formation and development of a thrombus or blood clot in the blood vessel.
A dangerous life-threatening hypermetabolic condition characterized by high FEVER and dysfunction of the cardiovascular, the nervous, and the gastrointestinal systems.
An enzyme formed from PROTHROMBIN that converts FIBRINOGEN to FIBRIN.
Use of a thrombelastograph, which provides a continuous graphic record of the physical shape of a clot during fibrin formation and subsequent lysis.
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.
Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation.
Toxins closely associated with the living cytoplasm or cell wall of certain microorganisms, which do not readily diffuse into the culture medium, but are released upon lysis of the cells.
Clotting time of PLASMA mixed with a THROMBIN solution. It is a measure of the conversion of FIBRINOGEN to FIBRIN, which is prolonged by AFIBRINOGENEMIA, abnormal fibrinogen, or the presence of inhibitory substances, e.g., fibrin-fibrinogen degradation products, or HEPARIN. BATROXOBIN, a thrombin-like enzyme unaffected by the presence of heparin, may be used in place of thrombin.
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.
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.
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.
Bleeding or escape of blood from a vessel.
A condition of inadequate circulating red blood cells (ANEMIA) or insufficient HEMOGLOBIN due to premature destruction of red blood cells (ERYTHROCYTES).
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.
A progressive condition usually characterized by combined failure of several organs such as the lungs, liver, kidney, along with some clotting mechanisms, usually postinjury or postoperative.
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.
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 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.
Purplish or brownish red discoloration, easily visible through the epidermis, caused by hemorrhage into the tissues. When the size of the discolorization is >2-3 cm it is generally called Ecchymoses (ECCHYMOSIS).
A pathological condition manifested by failure to perfuse or oxygenate vital organs.
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.
Sepsis associated with HYPOTENSION or hypoperfusion despite adequate fluid resuscitation. Perfusion abnormalities may include, but are not limited to LACTIC ACIDOSIS; OLIGURIA; or acute alteration in mental status.
Agents that prevent clotting.
A clinical syndrome caused by heat stress, such as over-exertion in a hot environment or excessive exposure to sun. It is characterized by SWEATING, water (volume) depletion, salt depletion, cool clammy skin, NAUSEA, and HEADACHE.
Activated form of factor VII. Factor VIIa activates factor X in the extrinsic pathway of blood coagulation.
Severe systemic manifestation of trauma and ischemia involving soft tissues, principally skeletal muscle, due to prolonged severe crushing. It leads to increased permeability of the cell membrane and to the release of potassium, enzymes, and myoglobin from within cells. Ischemic renal dysfunction secondary to hypotension and diminished renal perfusion results in acute tubular necrosis and uremia.
Pathological processes of the LIVER.
Storage-stable glycoprotein blood coagulation factor that can be activated to factor Xa by both the intrinsic and extrinsic pathways. A deficiency of factor X, sometimes called Stuart-Prower factor deficiency, may lead to a systemic coagulation disorder.
Death and putrefaction of tissue usually due to a loss of blood supply.
A contagious disease caused by canine adenovirus (ADENOVIRUSES, CANINE) infecting the LIVER, the EYE, the KIDNEY, and other organs in dogs, other canids, and bears. Symptoms include FEVER; EDEMA; VOMITING; and DIARRHEA.
Measurement of hemoglobin concentration in blood.
Postmortem examination of the body.
An absence or deficiency in PROTEIN C which leads to impaired regulation of blood coagulation. It is associated with an increased risk of severe or premature thrombosis. (Stedman's Med. Dict., 26th ed.)
Amino derivatives of caproic acid. Included under this heading are a broad variety of acid forms, salts, esters, and amides that contain the amino caproic acid structure.
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.
Extravasation of blood into the skin, resulting in a nonelevated, rounded or irregular, blue or purplish patch, larger than a petechia.
Inflammation of a vein, often a vein in the leg. Phlebitis associated with a blood clot is called (THROMBOPHLEBITIS).
The co-occurrence of pregnancy and a blood disease (HEMATOLOGIC DISEASES) which involves BLOOD CELLS or COAGULATION FACTORS. The hematologic disease may precede or follow FERTILIZATION and it may or may not have a deleterious effect on the pregnant woman or FETUS.
An operation for the continuous emptying of ascitic fluid into the venous system. Fluid removal is based on intraperitoneal and intrathoracic superior vena cava pressure differentials and is performed via a pressure-sensitive one-way valve connected to a tube traversing the subcutaneous tissue of the chest wall to the neck where it enters the internal jugular vein and terminates in the superior vena cava. It is used in the treatment of intractable ascites.
A disorder of HEMOSTASIS in which there is a tendency for the occurrence of THROMBOSIS.

Fitzgerald factor (high molecular weight kininogen) clotting activity in human plasma in health and disease in various animal plasmas. (1/581)

Fitzgerald factor (high molecular weight kininogen) is an agent in normal human plasma that corrects the impaired in vitro surface-mediated plasma reactions of blood coagulation, fibrinolysis, and kinin generation observed in Fitzgerald trait plasma. To assess the possible pathophysiologic role of Fitzgerald factor, its titer was measured by a functional clot-promoting assay. Mean +/- SD in 42 normal adults was 0.99+/-0.25 units/ml, one unit being the activity in 1 ml of normal pooled plasma. No difference in titer was noted between normal men and women, during pregnancy, or after physical exercise. Fitzgerald factor activity was significantly reduced in the plasmas of eight patients with advanced hepatic cirrhosis (0.40+/-0.09 units/ml) and of ten patients with disseminated intravascular coagulation (0.60+/-0.30 units/ml), but was normal in plasmas of patients with other congenital clotting factor deficiencies, nephrotic syndrome, rheumatoid arthritis, systemic lupus erythematosus, or sarcoidosis, or under treatment with warfarin. The plasmas of 21 mammalian species tested appeared to contain Fitzgerald factor activity, but those of two avian, two repitilian, and one amphibian species did not correct the coagulant defect in Fitzgerald trait plasmas.  (+info)

Transcatheter arterial embolization for impending rupture of an isolated internal iliac artery aneurysm complicated with disseminated intravascular coagulation. (2/581)

A 90-year-old male, with impending rupture of an isolated internal iliac artery aneurysm (IIAA) complicated with disseminated intravascular coagulation (DIC) was successfully treated with transcatheter arterial embolization (TAE). After TAE, enlargement of the aneurysm was arrested and coagulation-fibrinolytic abnormalities induced by DIC improved without severe complications. Although IIAA is relatively rare, the post-operative mortality of patients with ruptures is reportedly high. We assessed the usefulness of this procedure for impending rupture of IIAA, especially for patients in high risk groups.  (+info)

Hemolysis associated with 25% human albumin diluted with sterile water--United States, 1994-1998. (3/581)

Since 1994, a shortage of 5% human albumin, a product used off-label during therapeutic plasma exchange (TPE), has existed in the United States. Because of this shortage, hospital pharmacists may prepare 5% solution of human albumin by diluting 25% human albumin with 0.9% NaCl or, when sodium load is a concern, 5% dextrose. However, if sterile water alone is used as the diluent, the osmolarity (tonicity) of the albumin solution is reduced and may cause hemolysis in recipients. This report describes two of 10 episodes of hemolysis (one fatal) among persons who received 25% human albumin diluted with sterile water and emphasizes that sterile water alone should not be used to dilute albumin.  (+info)

Inflammation, sepsis, and coagulation. (4/581)

The molecular links between inflammation and coagulation are unquestioned. Inflammation promotes coagulation by leading to intravascular tissue factor expression, eliciting the expression of leukocyte adhesion molecules on the intravascular cell surfaces, and down regulating the fibrinolytic and protein C anticoagulant pathways. Thrombin, in turn, can promote inflammatory responses. This creates a cycle that logically progresses to vascular injury as occurs in septic shock. Most complex systems are regulated by product inhibition. This inflammation-coagulation cycle seems to follow this same principle with the protein C pathway serving as the regulatory mechanism. The molecular basis by which the protein C pathway functions as an anticoagulant is relatively well established compared to the mechanisms involved in regulating inflammation. As one approach to identifying the mechanisms involved in regulating inflammation, we set out to identify novel receptors that could modulate the specificity of APC in a manner analogous to the mechanisms by which thrombomodulin modulates thrombin specificity. This approach led to the identification of an endothelial cell protein C receptor (EPCR). To understand the mechanism, we obtained a crystal structure of APC (lacking the Gla domain). The crystal structure reveals a deep groove in a location analogous to anion binding exosite 1 of thrombin, the location of interaction for thrombomodulin, platelet thrombin receptor and fibrinogen. Thrombomodulin blocks the activation of platelets and fibrinogen without blocking reactivity with chromogenic substrates or inhibitors. Similarly, in solution, EPCR blocks factor Va inactivation without modulating reactivity with protease inhibitors. Thus, these endothelial cell receptors for the protein C system share many properties in common including the ability to be modulated by inflammatory cytokines. Current studies seek to identify the substrate for the APC-EPCR complex as the next step in elucidating the mechanisms by which the protein C pathway modulates the response to injury and inflammation.  (+info)

Incidence and possible reasons for discordant results between positive FDP and negative D-dimer latex assays in clinical specimens. (5/581)

In general, FDP and D-dimer values have a correlation in clinical conditions associated with disseminated intravascular coagulation(DIC) or coagulation activation. However, there are some patients with discordant results who demonstrate elevated FDP and negative D-dimer results by latex agglutination assays. The incidence and possible reasons for the discordance between FDP and D-dimer results were investigated through simultaneous measurements (n = 763) from clinical patients with suspected DIC or coagulation activation. 24.8% (189/763) of samples with elevated FDP were negative for D-dimer assays by the latex agglutination method. Further detailed analysis on randomly-selected discordant samples (n = 41) revealed that the most common reason for the discordance was the lower sensitivity of the semiquantitative latex agglutination method for D-dimer, compared with quantitative enzyme or other latex immunoassay. The other contributing factors to the discordance were accelerated fibrinogenolysis without secondary fibrinolysis, elevated soluble fibrin monomer and rheumatoid factor.  (+info)

Hypercalcemia and parathyroid hormone-related protein in a dog with undifferentiated nasal carcinoma. (6/581)

Hypercalcemia was discovered in a 7-year-old, castrated male basset hound with a suspected nasal tumor. The dog died the day after admission and nasal carcinoma and disseminated intravascular coagulation were diagnosed on postmortem. Detectable levels of serum PTHrP support a diagnosis of hypercalcemia of malignancy.  (+info)

Review: infectious diseases and coagulation disorders. (7/581)

Infection, both bacterial and nonbacterial, may be associated with coagulation disorders, resulting in disseminated intravascular coagulation and multiorgan failure. In the last few decades a series of in vivo and in vitro studies has provided more insight into the pathogenetic mechanisms and the role of cytokines in these processes. Because of the growing interest in this field, the complexity of the subject, and the fact that many physicians must deal with a variety of infections, current data are reviewed on the association between infectious diseases and the coagulation system. Novel therapeutic intervention strategies that will probably become available in the near future are mentioned, along with those of special interest for infectious disorders for which only supportive care can be given.  (+info)

Disseminated thrombosis and bone infarction in female rats following inhalation exposure to 2-butoxyethanol. (8/581)

Groups of 10 male and 10 female F344/N rats were exposed to 0, 31, 62.5, 125, 250, and 500 ppm of 2-butoxyethanol (BE) by inhalation, 6 hr/day, 5 days/wk, for 13 wk. Four moribund female rats from the 500 ppm group were sacrificed during the first 4 days of exposure, and 1 moribund female from the same group was sacrificed during week 5. Dark irregular mottling and/or loss of the distal tail were noted in sacrificed moribund rats. Similar gross lesions were noted in the terminally sacrificed females exposed to 500 ppm BE. Histologic changes noted in the day 4 sacrificed moribund rats included disseminated thrombosis involving the coccygeal vertebrae, cardiac atrium, lungs, liver, pulp of the incisor teeth, and the submucosa of the anterior section of the nasal cavity. Alterations noted in coccygeal vertebrae from the 500 ppm sacrificed moribund rats included ischemic necrosis and/or degeneration of bone marrow cells, bone-lining cells, osteocytes (within cortical and trabecular bone), and chondrocytes (both articular and growth plate), changes that are consistent with an infarction process. The moribund female rat that was sacrificed during week 5 and those female rats treated with 500 ppm and sacrificed following 13 wk of treatment lacked thrombi, but they had coccygeal vertebral changes consistent with prior infarction and transient or complete bone growth arrest. No bone lesions or thrombi were noted in the male rats treated with the same doses of BE. In conclusion, exposure to 500 ppm BE vapors caused acute disseminated thrombosis and bone infarction in female rats. Possible pathogenic mechanisms are discussed.  (+info)

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.

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 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.

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.

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.

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.

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.

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.

The Shwartzman phenomenon is a rare but serious condition characterized by the development of thrombotic vasculopathy in multiple organs. It is typically divided into two phases: the local reaction phase and the systemic reaction phase. The local reaction phase occurs after the injection of a large dose of bacterial endotoxin (such as Escherichia coli) into the skin, which results in a localized inflammatory response. This is followed by the systemic reaction phase, which can occur 24-48 hours later and is characterized by the development of thrombosis and necrosis in various organs, including the kidneys, lungs, and brain.

The Shwartzman phenomenon is thought to be caused by the activation of the complement system and the coagulation cascade, which leads to the formation of blood clots and the destruction of blood vessels. It can occur as a complication of certain medical procedures (such as intravenous pyelograms) or infections, and it is often seen in patients with compromised immune systems.

The Shwartzman phenomenon is named after the Russian-American physician, Maurice Shwartzman, who first described the condition in 1928.

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.

An amniotic fluid embolism (AFE) is a rare but serious condition that can occur during pregnancy, labor, or shortly after delivery. It occurs when amniotic fluid, fetal cells, hair, or other debris enter the mother's bloodstream and block the flow of blood to the lungs or other parts of the body. This can cause a range of symptoms including sudden shortness of breath, rapid heartbeat, low blood pressure, chills, and in severe cases, cardiac arrest or seizures. AFE is a medical emergency that requires immediate treatment.

The exact causes of amniotic fluid embolism are not well understood, but it is thought to occur when there is a disruption in the placental barrier that allows amniotic fluid and fetal debris to enter the mother's bloodstream. Risk factors for AFE include advanced maternal age, cesarean delivery, placenta previa, and other pregnancy complications.

Treatment for AFE typically involves supportive care, such as oxygen therapy, medications to support blood pressure and heart function, and in some cases, surgery to remove the blockage from the blood vessels. Despite treatment, AFE can be a life-threatening condition with significant morbidity and mortality rates.

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.

Gabexate is a medicinal drug that belongs to the class of agents known as serine protease inhibitors. It is used in the treatment and prevention of inflammation and damage to tissues caused by various surgical procedures, pancreatitis, and other conditions associated with the activation of proteolytic enzymes.

Gabexate works by inhibiting the activity of certain enzymes such as trypsin, chymotrypsin, and thrombin, which play a key role in the inflammatory response and blood clotting cascade. By doing so, it helps to reduce the release of inflammatory mediators, prevent further tissue damage, and promote healing.

Gabexate is available in various forms, including injectable solutions and enteric-coated tablets, and its use is typically reserved for clinical settings under the supervision of a healthcare professional. As with any medication, it should be used only under the direction of a qualified medical practitioner, and its potential benefits and risks should be carefully weighed against those of other available treatment options.

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.

Kidney cortex necrosis is a serious condition characterized by the death (necrosis) of cells in the outer part (cortex) of the kidneys, usually as a result of an interruption in blood flow. This can occur due to various reasons such as severe shock, blood clots, or complications from pregnancy. The necrosis of kidney cortical tissue can lead to acute renal failure, which is a life-threatening situation requiring immediate medical attention and intensive care.

The death of kidney cells in the cortex disrupts the normal functioning of the kidneys, impairing their ability to filter waste products and excess fluids from the blood. This can result in the accumulation of harmful substances in the body and an imbalance of electrolytes, which can be life-threatening if left untreated.

Kidney cortex necrosis is typically diagnosed through a combination of clinical evaluation, laboratory tests, and imaging studies such as ultrasound or CT scan. Treatment usually involves supportive care, including dialysis to replace the kidneys' function until they can recover on their own or until a transplant can be performed. In some cases, the damage to the kidneys may be permanent, leading to chronic renal failure and the need for long-term dialysis or transplantation.

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.

Interventional ultrasonography is a medical procedure that involves the use of real-time ultrasound imaging to guide minimally invasive diagnostic and therapeutic interventions. This technique combines the advantages of ultrasound, such as its non-ionizing nature (no radiation exposure), relatively low cost, and portability, with the ability to perform precise and targeted procedures.

In interventional ultrasonography, a specialized physician called an interventional radiologist or an interventional sonographer uses high-frequency sound waves to create detailed images of internal organs and tissues. These images help guide the placement of needles, catheters, or other instruments used during the procedure. Common interventions include biopsies (tissue sampling), fluid drainage, tumor ablation, and targeted drug delivery.

The real-time visualization provided by ultrasonography allows for increased accuracy and safety during these procedures, minimizing complications and reducing recovery time compared to traditional surgical approaches. Additionally, interventional ultrasonography can be performed on an outpatient basis, further contributing to its appeal as a less invasive alternative in many clinical scenarios.

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.

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.

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).

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.

Sepsis is a life-threatening condition that arises when the body's response to an infection injures its own tissues and organs. It is characterized by a whole-body inflammatory state (systemic inflammation) that can lead to blood clotting issues, tissue damage, and multiple organ failure.

Sepsis happens when an infection you already have triggers a chain reaction throughout your body. Infections that lead to sepsis most often start in the lungs, urinary tract, skin, or gastrointestinal tract.

Sepsis is a medical emergency. If you suspect sepsis, seek immediate medical attention. Early recognition and treatment of sepsis are crucial to improve outcomes. Treatment usually involves antibiotics, intravenous fluids, and may require oxygen, medication to raise blood pressure, and corticosteroids. In severe cases, surgery may be required to clear the infection.

A "Blood Cell Count" is a medical laboratory test that measures the number of red blood cells (RBCs), white blood cells (WBCs), and platelets in a sample of blood. This test is often used as a part of a routine check-up or to help diagnose various medical conditions, such as anemia, infection, inflammation, and many others.

The RBC count measures the number of oxygen-carrying cells in the blood, while the WBC count measures the number of immune cells that help fight infections. The platelet count measures the number of cells involved in clotting. Abnormal results in any of these counts may indicate an underlying medical condition and further testing may be required for diagnosis and treatment.

A fatal outcome is a term used in medical context to describe a situation where a disease, injury, or illness results in the death of an individual. It is the most severe and unfortunate possible outcome of any medical condition, and is often used as a measure of the severity and prognosis of various diseases and injuries. In clinical trials and research, fatal outcome may be used as an endpoint to evaluate the effectiveness and safety of different treatments or interventions.

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.

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.

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.

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.

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.

A thyroid crisis, also known as thyrotoxic crisis or storm, is a rare but life-threatening condition characterized by an exaggerated response to the excess production of thyroid hormones (thyrotoxicosis). This condition can lead to severe hypermetabolic state, multi-organ dysfunction, and cardiovascular collapse if not promptly diagnosed and treated.

Thyroid crisis is often triggered by a stressful event, infection, or surgery in individuals with uncontrolled or poorly managed hyperthyroidism, particularly those with Graves' disease. The symptoms of thyroid crisis include high fever, tachycardia (rapid heart rate), hypertension (high blood pressure), agitation, confusion, delirium, vomiting, diarrhea, and sometimes coma.

The diagnosis of thyroid crisis is based on the clinical presentation, laboratory tests, and imaging studies. Treatment typically involves hospitalization in an intensive care unit, administration of medications to block the production and release of thyroid hormones, control heart rate and rhythm, correct electrolyte imbalances, and provide supportive care until the patient's condition stabilizes.

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).

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.

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).

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.

Endotoxins are toxic substances that are associated with the cell walls of certain types of bacteria. They are released when the bacterial cells die or divide, and can cause a variety of harmful effects in humans and animals. Endotoxins are made up of lipopolysaccharides (LPS), which are complex molecules consisting of a lipid and a polysaccharide component.

Endotoxins are particularly associated with gram-negative bacteria, which have a distinctive cell wall structure that includes an outer membrane containing LPS. These toxins can cause fever, inflammation, and other symptoms when they enter the bloodstream or other tissues of the body. They are also known to play a role in the development of sepsis, a potentially life-threatening condition characterized by a severe immune response to infection.

Endotoxins are resistant to heat, acid, and many disinfectants, making them difficult to eliminate from contaminated environments. They can also be found in a variety of settings, including hospitals, industrial facilities, and agricultural operations, where they can pose a risk to human health.

Thrombin time (TT) is a medical laboratory test that measures the time it takes for a clot to form after thrombin, an enzyme that converts fibrinogen to fibrin in the final step of the coagulation cascade, is added to a plasma sample. This test is used to evaluate the efficiency of the conversion of fibrinogen to fibrin and can be used to detect the presence of abnormalities in the coagulation system, such as the presence of heparin or dysfibrinogenemia. Increased thrombin time may indicate the presence of a systemic anticoagulant or a deficiency in fibrinogen.

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.

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.

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.

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.

Hemolytic anemia is a type of anemia that occurs when red blood cells are destroyed (hemolysis) faster than they can be produced. Red blood cells are essential for carrying oxygen throughout the body. When they are destroyed, hemoglobin and other cellular components are released into the bloodstream, which can lead to complications such as kidney damage and gallstones.

Hemolytic anemia can be inherited or acquired. Inherited forms of the condition may result from genetic defects that affect the structure or function of red blood cells. Acquired forms of hemolytic anemia can be caused by various factors, including infections, medications, autoimmune disorders, and certain medical conditions such as cancer or blood disorders.

Symptoms of hemolytic anemia may include fatigue, weakness, shortness of breath, pale skin, jaundice (yellowing of the skin and eyes), dark urine, and a rapid heartbeat. Treatment for hemolytic anemia depends on the underlying cause and may include medications, blood transfusions, or surgery.

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.

Multiple Organ Failure (MOF) is a severe condition characterized by the dysfunction or failure of more than one organ system in the body. It often occurs as a result of serious illness, trauma, or infection, such as sepsis. The organs that commonly fail include the lungs, kidneys, liver, and heart. This condition can lead to significant morbidity and mortality if not promptly diagnosed and treated.

The definition of MOF has evolved over time, but a widely accepted one is the "Sequential Organ Failure Assessment" (SOFA) score, which evaluates six organ systems: respiratory, coagulation, liver, cardiovascular, renal, and neurologic. A SOFA score of 10 or more indicates MOF, and a higher score is associated with worse outcomes.

MOF can be classified as primary or secondary. Primary MOF occurs when the initial insult directly causes organ dysfunction, such as in severe trauma or septic shock. Secondary MOF occurs when the initial injury or illness has been controlled, but organ dysfunction develops later due to ongoing inflammation and other factors.

Early recognition and aggressive management of MOF are crucial for improving outcomes. Treatment typically involves supportive care, such as mechanical ventilation, dialysis, and medication to support cardiovascular function. In some cases, surgery or other interventions may be necessary to address the underlying cause of organ dysfunction.

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.

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.

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.

Purpura is a medical term that refers to the appearance of purple-colored spots on the skin or mucous membranes, caused by bleeding underneath the skin due to various factors such as blood clotting disorders, vasculitis (inflammation of the blood vessels), severe thrombocytopenia (low platelet count), or use of certain medications. These spots can vary in size and shape, ranging from small pinpoint hemorrhages (petechiae) to larger, irregularly shaped patches (ecchymoses). The bleeding is usually not caused by trauma or injury to the area. It's important to consult a healthcare professional if you notice any unexplained purpuric spots on your skin or mucous membranes, as they can indicate an underlying medical condition that requires further evaluation and treatment.

In medical terms, shock is a life-threatening condition that occurs when the body is not getting enough blood flow or when the circulatory system is not functioning properly to distribute oxygen and nutrients to the tissues and organs. This results in a state of hypoxia (lack of oxygen) and cellular dysfunction, which can lead to multiple organ failure and death if left untreated.

Shock can be caused by various factors such as severe blood loss, infection, trauma, heart failure, allergic reactions, and severe burns. The symptoms of shock include low blood pressure, rapid pulse, cool and clammy skin, rapid and shallow breathing, confusion, weakness, and a bluish color to the lips and nails. Immediate medical attention is required for proper diagnosis and treatment of shock.

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.

Septic shock is a serious condition that occurs as a complication of an infection that has spread throughout the body. It's characterized by a severe drop in blood pressure and abnormalities in cellular metabolism, which can lead to organ failure and death if not promptly treated.

In septic shock, the immune system overreacts to an infection, releasing an overwhelming amount of inflammatory chemicals into the bloodstream. This leads to widespread inflammation, blood vessel dilation, and leaky blood vessels, which can cause fluid to leak out of the blood vessels and into surrounding tissues. As a result, the heart may not be able to pump enough blood to vital organs, leading to organ failure.

Septic shock is often caused by bacterial infections, but it can also be caused by fungal or viral infections. It's most commonly seen in people with weakened immune systems, such as those who have recently undergone surgery, have chronic medical conditions, or are taking medications that suppress the immune system.

Prompt diagnosis and treatment of septic shock is critical to prevent long-term complications and improve outcomes. Treatment typically involves aggressive antibiotic therapy, intravenous fluids, vasopressors to maintain blood pressure, and supportive care in an intensive care unit (ICU).

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.

Heat exhaustion is a condition characterized by excessive loss of water and salt, typically through heavy sweating, leading to physical symptoms such as weakness, dizziness, cool moist skin with goose bumps when in a hot environment, and a rapid, weak pulse. It can also cause nausea, headache, and fainting. Heat exhaustion is less severe than heat stroke but should still be treated as a medical emergency to prevent progression to the more serious condition. The primary treatment for heat exhaustion includes restoring water and salt balance through oral or intravenous rehydration, cooling the body with cold compresses or a cool bath, and removing the person from the hot environment.

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.

Crush syndrome, also known as traumatic rhabdomyolysis, is a medical condition that occurs when a significant amount of muscle tissue is damaged or destroyed, releasing large amounts of intracellular contents into the circulation. This can happen due to prolonged compression of muscles, often seen in cases of entrapment in debris or heavy objects following natural disasters, accidents, or other traumatic events.

The crush syndrome is characterized by a triad of symptoms:

1. Muscle injury and breakdown (rhabdomyolysis) leading to the release of muscle contents such as potassium, myoglobin, creatine kinase, and uric acid into the bloodstream.
2. Electrolyte imbalances, particularly hyperkalemia (elevated potassium levels), which can cause cardiac arrhythmias and cardiac arrest if not promptly treated.
3. Acute kidney injury (AKI) due to myoglobinuria, where the released myoglobin from damaged muscle tissue clogs the renal tubules in the kidneys, impairing their function and potentially leading to acute renal failure.

Immediate medical intervention is crucial for managing crush syndrome, which includes aggressive fluid resuscitation, close monitoring of electrolyte levels, and supportive care for kidney function. In some cases, dialysis may be required to support the kidneys until they recover.

Liver diseases refer to a wide range of conditions that affect the normal functioning of the liver. The liver is a vital organ responsible for various critical functions such as detoxification, protein synthesis, and production of biochemicals necessary for digestion.

Liver diseases can be categorized into acute and chronic forms. Acute liver disease comes on rapidly and can be caused by factors like viral infections (hepatitis A, B, C, D, E), drug-induced liver injury, or exposure to toxic substances. Chronic liver disease develops slowly over time, often due to long-term exposure to harmful agents or inherent disorders of the liver.

Common examples of liver diseases include hepatitis, cirrhosis (scarring of the liver tissue), fatty liver disease, alcoholic liver disease, autoimmune liver diseases, genetic/hereditary liver disorders (like Wilson's disease and hemochromatosis), and liver cancers. Symptoms may vary widely depending on the type and stage of the disease but could include jaundice, abdominal pain, fatigue, loss of appetite, nausea, and weight loss.

Early diagnosis and treatment are essential to prevent progression and potential complications associated with liver diseases.

Factor X is a protein that is essential for blood clotting, also known as coagulation. It is an enzyme that plays a crucial role in the coagulation cascade, which is a series of chemical reactions that lead to the formation of a blood clot. Factor X is activated by one of two pathways: the intrinsic pathway, which is initiated by damage to the blood vessels, or the extrinsic pathway, which is triggered by the release of tissue factor from damaged cells. Once activated, Factor X converts prothrombin to thrombin, which then converts fibrinogen to fibrin to form a stable clot.

Inherited deficiencies in Factor X can lead to bleeding disorders, while increased levels of Factor X have been associated with an increased risk of thrombosis or blood clots. Therefore, maintaining appropriate levels of Factor X is important for the proper balance between bleeding and clotting in the body.

Gangrene is a serious and potentially life-threatening condition that occurs when there is a loss of blood flow to a specific area of the body, resulting in tissue death. It can be caused by various factors such as bacterial infections, trauma, diabetes, vascular diseases, and smoking. The affected tissues may become discolored, swollen, and emit a foul odor due to the accumulation of bacteria and toxins.

Gangrene can be classified into two main types: dry gangrene and wet (or moist) gangrene. Dry gangrene develops slowly and is often associated with peripheral arterial disease, which reduces blood flow to the extremities. The affected area turns black and shriveled as it dries out. Wet gangrene, on the other hand, progresses rapidly due to bacterial infections that cause tissue breakdown and pus formation. This type of gangrene can spread quickly throughout the body, leading to severe complications such as sepsis and organ failure if left untreated.

Treatment for gangrene typically involves surgical removal of the dead tissue (debridement), antibiotics to control infections, and sometimes revascularization procedures to restore blood flow to the affected area. In severe cases where the infection has spread or the damage is irreversible, amputation of the affected limb may be necessary to prevent further complications and save the patient's life.

Infectious canine hepatitis is a viral disease in dogs caused by canine adenovirus type 1 (CAV-1). The disease primarily affects the liver, but other organs such as the kidneys, eyes, and respiratory system may also be involved.

The virus is transmitted through direct contact with infected dogs or their urine, feces, saliva, or ocular/nasal discharge. It can also be spread through contaminated objects, water, or food. After infection, the virus incubates for 4-7 days before signs of illness appear.

Clinical signs of infectious canine hepatitis can vary widely in severity, from mild to severe. They may include fever, lethargy, loss of appetite, vomiting, diarrhea, abdominal pain, increased thirst and urination, jaundice (yellowing of the skin, mucous membranes, and whites of the eyes), and cloudiness or bluish discoloration of the cornea. In severe cases, neurological signs such as seizures or coma may occur.

Treatment for infectious canine hepatitis is primarily supportive, as there is no specific antiviral therapy available. Treatment may include fluid therapy to maintain hydration and electrolyte balance, nutritional support, medications to control vomiting and diarrhea, and management of any secondary bacterial infections that may develop.

Prevention of infectious canine hepatitis is achieved through vaccination with a modified-live or inactivated vaccine containing CAV-1. Puppies should receive their first vaccination at 6-8 weeks of age, followed by a booster at 10-12 weeks and another booster at 14-16 weeks. Annual revaccination is recommended to maintain immunity.

Hemoglobinometry is a method used to measure the amount or concentration of hemoglobin (Hb) in blood. Hemoglobin is a protein in red blood cells that carries oxygen throughout the body. Hemoglobinometry is typically performed on a sample of whole blood and can be done using various methods, including spectrophotometry, colorimetry, or automated analyzers.

The results of hemoglobinometry are reported in units of grams per deciliter (g/dL) or grams per liter (g/L). Normal values for hemoglobin concentration vary depending on factors such as age, sex, and altitude, but in general, a healthy adult male should have a hemoglobin level between 13.5 and 17.5 g/dL, while a healthy adult female should have a level between 12.0 and 15.5 g/dL.

Hemoglobinometry is an important diagnostic tool in the evaluation of various medical conditions, including anemia, polycythemia, and respiratory disorders. It can help identify the cause of symptoms such as fatigue, shortness of breath, or dizziness and guide treatment decisions.

An autopsy, also known as a post-mortem examination or obduction, is a medical procedure in which a qualified professional (usually a pathologist) examines a deceased person's body to determine the cause and manner of death. This process may involve various investigative techniques, such as incisions to study internal organs, tissue sampling, microscopic examination, toxicology testing, and other laboratory analyses. The primary purpose of an autopsy is to gather objective evidence about the medical conditions and factors contributing to the individual's demise, which can be essential for legal, insurance, or public health purposes. Additionally, autopsies can provide valuable insights into disease processes and aid in advancing medical knowledge.

Protein C deficiency is a genetic disorder that affects the body's ability to control blood clotting. Protein C is a protein in the blood that helps regulate the formation of blood clots. When blood clots form too easily or do not dissolve properly, they can block blood vessels and lead to serious medical conditions such as deep vein thrombosis (DVT) or pulmonary embolism (PE).

People with protein C deficiency have lower than normal levels of this protein in their blood, which can increase their risk of developing abnormal blood clots. The condition is usually inherited and present from birth, but it may not cause any symptoms until later in life, such as during pregnancy, after surgery, or due to other factors that increase the risk of blood clots.

Protein C deficiency can be classified into two types: type I and type II. Type I deficiency is characterized by lower than normal levels of both functional and immunoreactive protein C in the blood. Type II deficiency is characterized by normal or near-normal levels of immunoreactive protein C, but reduced functional activity.

Protein C deficiency can be diagnosed through blood tests that measure the level and function of protein C in the blood. Treatment may include anticoagulant medications to prevent blood clots from forming or dissolve existing ones. Regular monitoring of protein C levels and careful management of risk factors for blood clots are also important parts of managing this condition.

Aminocaproates are a group of chemical compounds that contain an amino group and a carboxylic acid group, as well as a straight or branched alkyl chain with 6-10 carbon atoms. They are often used in medical settings as anti-fibrinolytic agents, which means they help to prevent the breakdown of blood clots.

One example of an aminocaproate is epsilon-aminocaproic acid (EACA), which is a synthetic analogue of the amino acid lysine. EACA works by inhibiting the activation of plasminogen to plasmin, which is an enzyme that breaks down blood clots. By doing so, EACA can help to reduce bleeding and improve clot stability in certain medical conditions, such as hemophilia or following surgery.

Other aminocaproates include tranexamic acid (TXA) and 4-aminoethylbenzoic acid (AEBA), which also have anti-fibrinolytic properties and are used in similar clinical settings. However, it's important to note that these medications can increase the risk of thrombosis (blood clots) if not used properly, so they should only be administered under the close supervision of a healthcare provider.

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).

Ecchymosis is a medical term that refers to a discoloration of the skin caused by the leakage of blood from ruptured blood vessels into the tissues beneath. It is typically caused by trauma or injury to the affected area, which results in the escape of blood from the damaged blood vessels. The escaped blood collects under the skin, causing a bruise or a purple, blue, or blackish patch on the skin's surface.

Ecchymosis can occur anywhere on the body and can vary in size and shape depending on the extent of the injury. While ecchymosis is generally harmless and resolves on its own within a few days to a week, it can be a sign of an underlying medical condition, such as a bleeding disorder or a blood vessel abnormality. In these cases, further evaluation and treatment may be necessary.

Phlebitis is a medical term that refers to the inflammation of a vein, usually occurring in the legs. The inflammation can be caused by blood clots (thrombophlebitis) or other conditions that cause irritation and swelling in the vein's lining. Symptoms may include redness, warmth, pain, and swelling in the affected area. In some cases, phlebitis may lead to serious complications such as deep vein thrombosis (DVT) or pulmonary embolism (PE), so it is essential to seek medical attention if you suspect you have this condition.

Hematologic pregnancy complications refer to disorders related to the blood and blood-forming tissues that occur during pregnancy. These complications can have serious consequences for both the mother and the fetus if not properly managed. Some common hematologic pregnancy complications include:

1. Anemia: A condition characterized by a decrease in the number of red blood cells or hemoglobin in the blood, which can lead to fatigue, weakness, and shortness of breath. Iron-deficiency anemia is the most common type of anemia during pregnancy.
2. Thrombocytopenia: A condition characterized by a decrease in the number of platelets (cells that help blood clot) in the blood. Mild thrombocytopenia is relatively common during pregnancy, but severe thrombocytopenia can increase the risk of bleeding during delivery.
3. Gestational thrombotic thrombocytopenic purpura (GTTP): A rare but serious disorder that can cause blood clots to form in small blood vessels throughout the body, leading to a decrease in the number of platelets and red blood cells. GTTP can cause serious complications such as stroke, kidney failure, and even death if not promptly diagnosed and treated.
4. Disseminated intravascular coagulation (DIC): A condition characterized by abnormal clotting and bleeding throughout the body. DIC can be triggered by various conditions such as severe infections, pregnancy complications, or cancer.
5. Hemolysis, elevated liver enzymes, and low platelets (HELLP) syndrome: A serious complication of pregnancy that can cause damage to the liver and lead to bleeding. HELLP syndrome is often associated with preeclampsia, a condition characterized by high blood pressure and damage to organs such as the liver and kidneys.

It's important for pregnant women to receive regular prenatal care to monitor for these and other potential complications, and to seek prompt medical attention if any concerning symptoms arise.

A Peritoneovenous Shunt is a medical device used to treat severe ascites, a condition characterized by the accumulation of excess fluid in the abdominal cavity. The shunt consists of a small tube or catheter that is surgically implanted into the abdominal cavity and connected to another tube that is inserted into a vein, usually in the chest or neck.

The shunt works by allowing the excess fluid in the abdomen to flow through the tube and into the bloodstream, where it can be eliminated from the body through the kidneys. This helps to alleviate the symptoms of ascites, such as abdominal pain and swelling, and can improve the patient's quality of life.

Peritoneovenous shunts are typically used in patients who have not responded to other treatments for ascites, such as diuretics or paracentesis (a procedure in which excess fluid is drained from the abdomen using a needle and syringe). While peritoneovenous shunts can be effective in managing ascites, they do carry some risks, including infection, bleeding, and blockage of the shunt. As with any surgical procedure, it's important for patients to discuss the potential benefits and risks with their healthcare provider before deciding whether a peritoneovenous shunt is right for them.

Thrombophilia is a medical condition characterized by an increased tendency to form blood clots (thrombi) due to various genetic or acquired abnormalities in the coagulation system. These abnormalities can lead to a hypercoagulable state, which can cause thrombosis in both veins and arteries. Commonly identified thrombophilias include factor V Leiden mutation, prothrombin G20210A mutation, antithrombin deficiency, protein C deficiency, and protein S deficiency.

Acquired thrombophilias can be caused by various factors such as antiphospholipid antibody syndrome (APS), malignancies, pregnancy, oral contraceptive use, hormone replacement therapy, and certain medical conditions like inflammatory bowel disease or nephrotic syndrome.

It is essential to diagnose thrombophilia accurately, as it may influence the management of venous thromboembolism (VTE) events and guide decisions regarding prophylactic anticoagulation in high-risk situations.

"Disseminated Intravascular Coagulation". National Heart, Lung And Blood Institute. Retrieved 12 July 2021. "Disseminated ... "Disseminated Intravascular Coagulation , NHLBI, NIH". www.nhlbi.nih.gov. Retrieved 20 December 2017. "Disseminated ... Disseminated intravascular coagulation (DIC) is a condition in which blood clots form throughout the body, blocking small blood ... Disseminated intravascular coagulation Archived 2010-01-30 at the Wayback Machine at eMedicine, 10 September 2009 Matsuda, T ( ...
"Disseminated Intravascular Coagulation". The Lecturio Medical Concept Library. Archived from the original on 12 July 2021. ... disseminated intravascular coagulation, heparin-induced thrombocytopenia). An increase in platelet count leading to elevated ... Coagulation can physically trap invading microbes in blood clots. Also, some products of the coagulation system can contribute ... Disorders of coagulation are disease states which can result in problems with hemorrhage, bruising, or thrombosis. Coagulation ...
"Disseminated Intravascular Coagulation , National Heart, Lung, and Blood Institute (NHLBI)". www.nhlbi.nih.gov. Retrieved 2018- ... and suspected disseminated intravascular coagulation: an overactivity of clotting proteins that can lead to eventual hemorrhage ...
Disseminated intravascular coagulation occurs and results in serious bleeding. The condition can also develop after elective ... 129-. ISBN 978-0-323-29639-7. "Disseminated Intravascular Coagulation". The Lecturio Medical Concept Library. Retrieved 12 July ... and profuse bleeding due to defects in blood coagulation. Though symptoms and signs can be profound, they also can be entirely ...
Disseminated intravascular coagulation (DIC), diffuse formation of blood clots throughout the blood vessels of the body, has ... "Disseminated Intravascular Coagulation , NHLBI, NIH". National Heart, Lung and Blood Institute. 8 October 2019. Archived from ... and related bleeding including disseminated intravascular coagulation and cerebral venous sinus thrombosis (CVST), noting any ...
Activation of the coagulation system may precipitate disseminated intravascular coagulation. High potassium levels may lead to ... Disseminated intravascular coagulation, another complication of rhabdomyolysis and other forms of critical illness, may be ... Disseminated intravascular coagulation generally resolves when the underlying causes are treated, but supportive measures are ... A second recognized complication is disseminated intravascular coagulation (DIC), a severe disruption in blood clotting that ...
Liberation of blood cell debris into the circulation will also cause disseminated intravascular coagulation. Patients receiving ... Costello RA, Nehring SM (2019). "Disseminated Intravascular Coagulation (DIC)". StatPearls. StatPearls Publishing. PMID ...
"Disseminated Intravascular Coagulation (DIC)". Fastbleep Medical Notes. Archived from the original on 2015-03-04. Retrieved ... Several microangiopathic diseases, including disseminated intravascular coagulation and thrombotic microangiopathies, generate ... "Schistocytes in disseminated intravscular coagulation". International Journal of Laboratory Hematology. 36 (4): 439-43. doi: ...
Solid tumors such as adenocarcinomas can contribute to both VTE and disseminated intravascular coagulation. In severe cases, ... Levi M, Scully M (February 2018). "How I treat disseminated intravascular coagulation". Blood. 131 (8): 845-54. doi:10.1182/ ... Clotting is activated by the coagulation cascade and the clearing of clots that are no longer needed is accomplished by the ... Reductions in fibrinolysis or increases in coagulation can increase the risk of DVT. DVT often develops in the calf veins and " ...
Disseminated intravascular coagulation - a widespread activation of clotting in the smaller blood vessels. Cerebrovascular ... "Disseminated intravascular coagulation (DIC): MedlinePlus Medical Encyclopedia". www.nlm.nih.gov. Retrieved 2015-06-25. "Stroke ...
Like many cancers, liver angiosarcoma can also cause disseminated intravascular coagulation (DIC). Most liver angiosarcoma ... "Management of disseminated intravascular coagulation in a patient with hepatic angiosarcoma". Medicine. 97 (47): e13321. doi: ... "Mysterious abdominal pain and disseminated intravascular coagulation due to hepatic angiosarcoma". Internal Medicine Journal. ... "Hepatic angiosarcoma associated with disseminated intravascular coagulation". Proceedings (Baylor University. Medical Center). ...
... levels are used as a predictive biomarker for the blood disorder disseminated intravascular coagulation and in the ... Asakura, Hidesaku; Ogawa, Haruhiko (2020). "COVID-19-associated coagulopathy and disseminated intravascular coagulation". ... or disseminated intravascular coagulation (DIC). For DVT and PE, there are possible various scoring systems that are used to ... because of the presence of thrombosis or disseminated intravascular coagulation. The D-dimer assay depends on the binding of a ...
The cardinal features of purpura investigations are the same as those of disseminated intravascular coagulation: prolonged ... The amount of fresh frozen plasma required to reverse disseminated intravascular coagulation associated with purpura fulminans ... Ghosh SK, Bandyopadhyay D, Dutta A (2009). "Purpura fulminans: a cutaneous marker of disseminated intravascular coagulation". ... In cases of severe inheritable protein C deficiency, purpura fulminans with disseminated intravascular coagulation manifests ...
"Ceftriaxone induced immune hemolytic anemia with disseminated intravascular coagulation". Indian Journal of Critical Care ...
Disseminated intravascular coagulation (DIC) is a possible sequela of HGE. As a result, this disease can cause severe damage. ...
Caesarean section is contraindicated in cases of disseminated intravascular coagulation. An obstetrician may need to divide the ...
Severe disseminated intravascular coagulation also can occur in severe envenomations. Early medical treatment and early access ...
"Blue Toe Syndrome as an Early Sign of Disseminated Intravascular Coagulation". Ann Dermatol. 28 (3): 400-1. doi:10.5021/ad. ...
... septic shock and syndrome of disseminated intravascular coagulation syndrome. Part 1". Annals of the Russian Academy of Medical ... This is a known risk in certain forms of vaccines injected intravenously but more generic terms like Disseminated intravascular ... coagulation and cytokine storm have largely replaced the term. Sanarelli married Maria Carmen Pons in Montevideo in 1898. In ...
"Disseminated intravascular coagulation caused by moojenactivase, a procoagulant snake venom metalloprotease". International ... it also caused Intravascular hemolysis. The venom has a lethal dose of 0.205 mg / kg for horses. The average yield for an adult ... consumption of fibrinogen and the plasma coagulation factors like Factor X and II, and thrombocytopenia, ...
Disseminated intravascular coagulation (DIC): Involving abnormal, excessive generation of thrombin and fibrin within the blood ... "Disseminated Intravascular Coagulation (DIC) - Hematology and Oncology - Merck Manuals Professional Edition". Merck Manuals ... and disseminated intravascular coagulation (DIC). It may also be a rare adverse effect to ceftriaxone. Hypoprothrombinemia is ... Vitamin K-dependent coagulation factors have a very short half-life, sometimes leading to a deficiency when a depletion of ...
The possibility of disseminated intravascular coagulation, a dangerous and difficult-to-manage condition, is concerning. ... The coagulopathy can progress to disseminated intravascular coagulation and even death. Hemolytic anemia secondary to ...
Complications may include disseminated intravascular coagulation, placental abruption, and kidney failure. The cause is unknown ... "A syndrome of liver damage and intravascular coagulation in the last trimester of normotensive pregnancy. A clinical and ... During the coagulation cascade, fibrin is deposited in the liver and leads to hepatic sinusoidal obstruction and vascular ... Pritchard JA, Weisman R Jr, Ratnoff OD, Vosburgh GJ (Jan 1954). "Intravascular hemolysis, thrombocytopenia and other ...
In other cases, ARF is often caused by disseminated intravascular coagulation. In any case, antivenin therapy and intravenous ... It is more often the result of intravascular hemolysis, which occurs in about half of all cases. ... Of the more dangerous systemic symptoms, hemorrhage and coagulation defects are the most striking. Hematemesis, melena, ...
Vasculitis can occur, causing edema and potentially disseminated intravascular coagulation (DIC). Myocarditis, pericarditis, ...
... can be due to vasculitis or disseminated intravascular coagulation. Various other conditions have been ...
In other cases, ARF is often caused by disseminated intravascular coagulation. The Fer-de-lance or Terciopelo (Bothrops asper) ... usually in 2-4 days from complications following blood volume deficit and a disseminated intravascular coagulopathy), although ... Serious bites cause limbs to become immovably flexed as a result of significant hemorrhage or coagulation in the affected ... It is more often the result of intravascular hemolysis, which occurs in about half of all cases. ...
Rarely more severe symptoms occur including hemolysis, thrombocytopenia, and disseminated intravascular coagulation. ... Vorse, Hal; Seccareccio, Paul; Woodruff, Kay; Humphrey, G. Bennett (June 1972). "Disseminated intravascular coagulopathy ...
Disseminated intravascular coagulation occurs as the toxin interacts with the victim's body. One serious effect on envenomed ... Lonomia obliqua has a toxic venom which causes disseminated intravascular coagulation and a consumptive coagulopathy, which can ... It effectively reverses the coagulation disorders induced by Lonomia obliqua venom, and patients treated with this antiserum ... "Lonomia obliqua Caterpillar Spicules Trigger Human Blood Coagulation via Activation of Factor X and Prothrombin". Thrombosis ...
Lonomia obliqua has a toxic venom which causes disseminated intravascular coagulation and a consumptive coagulopathy, which can ... Disseminated intravascular coagulation occurs as the toxin interacts with the victim's body. One serious effect on envenomed ... disseminated intravascular coagulation and necrotizing fasciitis of the lower limbs, despite his serious condition, the victim ... During hospitalization, she developed serious systemic effects, such as intravascular hemolytic anemia evidenced by ...
"Disseminated Intravascular Coagulation". National Heart, Lung And Blood Institute. Retrieved 12 July 2021. "Disseminated ... "Disseminated Intravascular Coagulation , NHLBI, NIH". www.nhlbi.nih.gov. Retrieved 20 December 2017. "Disseminated ... Disseminated intravascular coagulation (DIC) is a condition in which blood clots form throughout the body, blocking small blood ... Disseminated intravascular coagulation Archived 2010-01-30 at the Wayback Machine at eMedicine, 10 September 2009 Matsuda, T ( ...
Disseminated intravascular coagulation (DIC) is a serious disorder in which the proteins that control blood clotting become ... Disseminated intravascular coagulation (DIC) is a serious disorder in which the proteins that control blood clotting become ... Levi M. Disseminated intravascular coagulation. In: Hoffman R, Benz EJ, Silberstein LE, et al, eds. Hematology: Basic ... Disseminated intravascular coagulation (DIC) is a serious disorder in which the proteins that control blood clotting become ...
... is characterized by systemic activation of blood coagulation, which results in generation and deposition of fibrin, leading to ... Consumption and subsequent exhaustion of coagulation proteins and pl... ... encoded search term (Disseminated Intravascular Coagulation (DIC)) and Disseminated Intravascular Coagulation (DIC) What to ... Causes of Chronic Disseminated Intravascular Coagulation. *Table 3. Main Features of Disseminated Intravascular Coagulation in ...
If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Centers RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.. ...
BACKGROUND--The pathological features of the lung in disseminated intravascular coagulation (DIC) have not been established. ... Incidence of pulmonary thromboembolism, infarction and haemorrhage in disseminated intravascular coagulation: a necroscopic ... Incidence of pulmonary thromboembolism, infarction and haemorrhage in disseminated intravascular coagulation: a necroscopic ... were 87 patients whose illnesses were complicated by DIC and 64 patients who showed no abnormalities of blood coagulation in ...
Disseminated Intravascular Coagulation (DIC) - Learn about the causes, symptoms, diagnosis & treatment from the Merck Manuals ... What is disseminated intravascular coagulation (DIC)? Coagulation is a word for clotting. Disseminated means throughout the ...
Oral submucous fibrosis--a chronic disseminated intravascular coagulation syndrome with local coagulopathy. ... Oral submucous fibrosis--a chronic disseminated intravascular coagulation syndrome with local coagulopathy. ...
Purpose: Advanced gastric cancer (AGC) rarely presents with disseminated intravascular coagulation (DIC) at the time of ... with methotrexate and 5-fluorouracil for chemotherapy-naive advanced gastric cancer with disseminated intravascular coagulation ...
... ... Disseminated intravascular coagulation induced by endotoxin in rabbits: effect of treatment with t-PA and urokinase. Dec 1, ... on endotoxin-induced disseminated intravascular coagulation (DIC) in the rabbit.. MATERIAL AND METHODS. DIC was induced by ... No doses of t-PA modified the changes appearing in blood coagulation. UK reduced the fibrinogen and factor XII consumption ...
Disseminated intravascular coagulation and secondary thrombotic microangiopathy can co-occur in Salmonella derby septicemia. ... Thrombotic microangiopathy should not be missed just because of the diagnosis of disseminated intravascular coagulation. Proper ... leading to the co-occurrence of disseminated intravascular coagulation and secondary thrombotic microangiopathy. She received ... Laboratory workup demonstrated coagulation disorder, hemolytic anemia, thrombocytopenia, and acute kidney injury, ...
Disseminated intravascular coagulation after isolated mild head injury Pereira EAC., Green AL., Chandran H., Joshi SM., ...
... is characterized by systemic activation of blood coagulation, which results in generation and deposition of fibrin, leading to ... Consumption and subsequent exhaustion of coagulation proteins and pl... ... encoded search term (Disseminated Intravascular Coagulation) and Disseminated Intravascular Coagulation What to Read Next on ... Causes of Chronic Disseminated Intravascular Coagulation. *Table 3. Main Features of Disseminated Intravascular Coagulation in ...
STUDY OBJECTIVE: Our aim was to document the following in patients with septic shock and disseminated intravascular coagulation ... The pathophysiology, diagnosis, and management of sepsis-associated disseminated intravascular coagulation.Toshiaki Iba et al. ... Septic shock, multiple organ failure, and disseminated intravascular coagulation. Compared patterns of antithrombin III, ...
Disseminated Intravascular Coagulation (DIC). Etiology. Relative Frequencies of Etiologies of Disseminated Intravascular ... Hemorrhage is More Common in Acute Disseminated Intravascular Coagulation (DIC) Than in Chronic Disseminated Intravascular ... Thrombosis is More Common in Chronic Disseminated Intravascular Coagulation (DIC) than in Acute Disseminated Intravascular ... Hemorrhage is More Common in Acute Disseminated Intravascular Coagulation (DIC) Than in Chronic Disseminated Intravascular ...
Beware of other conditions that can mimic disseminated intravascular coagulation:*******. *What other clinical manifestations ... Disseminated intravascular coagulation (DIC) is always secondary to some process that leads to pathologic and systemic ... Beware of other conditions that can mimic disseminated intravascular coagulation:. In a patient with an appropriate initiating ... "Towards definition, clinical and laboratory criteria, and a scoring system for disseminated intravascular coagulation". Thromb ...
Disseminated Intravascular Coagulation [see Warnings and Precautions (5.2)] * Amniotic Fluid Embolism [see Warnings and ... Disseminated Intravascular Coagulation Inform women that the use of CERVIDIL is associated with an increased risk of ... 5.2 Disseminated Intravascular Coagulation. CERVIDIL should be used with caution in women at high risk of postpartum ... Disseminated Intravascular Coagulation: Assess for evolving fibrinolysis in the immediate post-partum period. (5.2) ...
Learn Disseminated Intravascular Coagulation (DIC) Interventions for Nursing RN faster and easier with Picmonics unforgettable ... Disseminated Intravascular Coagulation (DIC) is an abnormal initiation of the clotting cascade due to an underlying disease or ... Disseminated Intravascular Coagulation (DIC) Interventions. Quiz. Picmonics rapid review multiple-choice quiz allows you to ... Disseminated Intravascular Coagulation (DIC) Interventions. Master Disseminated Intravascular Coagulation (DIC) Interventions ...
Coagulation and Disseminated Intravascular Coagulation. / Thorborg, Per A.J.; Boshkov, Lynn K. Critical Care. Mosby Inc., 2005 ... Coagulation and Disseminated Intravascular Coagulation. In Critical Care. Mosby Inc. 2005. p. 261-272 doi: 10.1016/B978-0-323- ... Thorborg, P. A. J., & Boshkov, L. K. (2005). Coagulation and Disseminated Intravascular Coagulation. In Critical Care (pp. 261- ... Thorborg, PAJ & Boshkov, LK 2005, Coagulation and Disseminated Intravascular Coagulation. in Critical Care. Mosby Inc., pp. 261 ...
Disseminated Intravascular Coagulation (DIC) - Learn about the causes, symptoms, diagnosis & treatment from the MSD Manuals - ... What is disseminated intravascular coagulation (DIC)? Coagulation is a word for clotting. Disseminated means throughout the ...
Disseminated Intravascular Coagulation [see Warnings and Precautions (5.2)] * Amniotic Fluid Embolism [see Warnings and ... 5.2 Disseminated Intravascular Coagulation 5.3 Amniotic Fluid Embolism Syndrome 5.4 Uterine Tachysystole and Uterine ... Disseminated Intravascular Coagulation Inform women that the use of CERVIDIL is associated with an increased risk of ... 5.2 Disseminated Intravascular Coagulation. CERVIDIL should be used with caution in women at high risk of postpartum ...
Is Early Hemorrhagic Smallpox Disseminated Intravascular Coagulation? Are High Case-Fatality Rates in Unvaccinated Pregnant ... This disease had all the hallmarks of disseminated intravascular coagulation (DIC). Patients had widespread hemorrhaging in the ... Is Early Hemorrhagic Smallpox Disseminated Intravascular Coagulation?. Smallpox was eradicated before cases of early ... This policy review addresses whether early hemorrhagic smallpox is disseminated intravascular coagulation and speculates about ...
Vincent, JL., Castro, P., Hunt, B.J. et al. Thrombocytopenia in the ICU: disseminated intravascular coagulation and thrombotic ... Thrombocytopenia in the ICU: disseminated intravascular coagulation and thrombotic microangiopathies-what intensivists need to ... Thrombocytopenia in the ICU: disseminated intravascular coagulation and thrombotic microangiopathies-what intensivists need to ... An algorithm to rapidly differentiate disseminated intravascular coagulation (DIC) from thrombotic thrombocytopenic purpura ( ...
Coagulation Disseminated Intravascular): Read more about Symptoms, Diagnosis, Treatment, Complications, Causes and Prognosis. ... Symptoms of Disseminated Intravascular Coagulation If you are affected by disseminated intravascular coagulation, some of the ... Disseminated intravascular coagulation is not a disease in itself but it is a complication which presents itself as an illness ... Symptoms of Disseminated Intravascular Coagulation Abnormal bleeding from anywhere in the body, possibly at several sites at ...
5.14 Disseminated Intravascular Coagulation (DIC). Because of the risk of disseminated intravascular coagulation with use of ... 5.14 Disseminated Intravascular Coagulation (DIC) 6 ADVERSE REACTIONS 6.1 Clinical Trials Experience 6.2 Postmarketing ... due to the risk of disseminated intravascular coagulation. Patients with systemic onset JRA should be monitored for the ... Co-morbid conditions such as coagulation disorders or concomitant use of warfarin, other anticoagulants, antiplatelet drugs (e. ...
Disseminated Intravascular Coagulation (DIC). Elevated DDi implies the involvement of fibrinolysis secondary to coagulation ... in case of disseminated intravascular coagulation: DIC). D-dimer determination is mainly used to rule out deep vein thrombosis ... During plasma coagulation, soluble fibrin is generated by the influence of thrombin on fibrinogen. The soluble fibrin is cross- ... D-Dimers is degradation products of fibrin, biomarker for activation of plasma coagulation and/or fibrinolysis. Yumizen G DDi 2 ...
Disseminated intravascular coagulation secondary to an aortoiliac aneurysm * García-Martínez, Ma.B. ...
We postulate that direct activation of the coagulation cascade by the intraventricular metastasis probably triggered the ... Disseminated Intravascular Coagulation (DIC) complicates up to 7% of malignancies, the commonest solid organ association being ... John, T., Davis, I.D. Ventricular metastasis resulting in disseminated intravascular coagulation. World J Surg Onc 3, 29 (2005 ... Disseminated Intravascular Coagulation (DIC) complicates up to 7% of malignancies, the commonest solid organ association being ...
Predictive Factors for Disseminated Intravascular Coagulation in Childhood Acute Lymphoblastic Leukemia. N. Songthawee, P. ... Songthawee N, Sripornsawan P, Chotsampancharoen T. Predictive Factors for Disseminated Intravascular Coagulation in Childhood ... abstracts.isth.org/abstract/predictive-factors-for-disseminated-intravascular-coagulation-in-childhood-acute-lymphoblastic- ... abstracts.isth.org/abstract/predictive-factors-for-disseminated-intravascular-coagulation-in-childhood-acute-lymphoblastic- ...
  • Oral submucous fibrosis--a chronic disseminated intravascular coagulation syndrome with local coagulopathy. (bmj.com)
  • In dilutional coagulopathy, the patient's PT, PTT, TT, and platelet count are all diluted because of massive infusion (several liters) of packed red blood cells, fresh frozen plasma (FFP), or crystalloid solutions which lack platelets and most coagulation factors. (infectiousdiseaseadvisor.com)
  • We postulate that direct activation of the coagulation cascade by the intraventricular metastasis probably triggered the coagulopathy in this patient. (biomedcentral.com)
  • Background: Disseminated Intravascular coagulopathy (DIC) has been reported following use of Misoprostol which is an old drug with new indications in Obstetrics and Gynecology. (bvsalud.org)
  • Method: This is to report a case of disseminated intravascular coagulopathy (DIC) associated with use of misoprostol for induction of labour and to call for extra vigilance in its use.Result: This was a case of 22-year old gravida 2 para 1 at 42 weeks gestation that was induced with 100?g of isoprostol and delivered a live female baby with good Apgar score. (bvsalud.org)
  • citation needed] Under homeostatic conditions, the body is maintained in a finely tuned balance of coagulation and fibrinolysis. (wikipedia.org)
  • In a state of homeostasis, the presence of plasmin is critical, as it is the central proteolytic enzyme of coagulation and is also necessary for the breakdown of clots, or fibrinolysis. (wikipedia.org)
  • citation needed] In DIC, the processes of coagulation and fibrinolysis are dysregulated, and the result is widespread clotting with resultant bleeding. (wikipedia.org)
  • Sarode R, Kessler CM. Coagulation and fibrinolysis. (medlineplus.gov)
  • Derangement of the fibrinolytic system further contributes to intravascular clot formation, but in some cases, accelerated fibrinolysis may cause severe bleeding. (medscape.com)
  • D-Dimers is degradation products of fibrin, biomarker for activation of plasma coagulation and/or fibrinolysis. (horiba.com)
  • Elevated DDi implies the involvement of fibrinolysis secondary to coagulation activation, which is very interesting in the diagnosis of DIC. (horiba.com)
  • Hence, a patient with disseminated intravascular coagulation (DIC) can present with a simultaneously occurring thrombotic and bleeding problem, which obviously complicates the proper treatment. (medscape.com)
  • This combination of thrombocytopenia and MAHA, in which thrombi form in the microvasculature and schistocytes develop from red cell destruction as they pass over these thrombi [ 2 ], occurs in patients with disseminated intravascular coagulation (DIC), but also in those with thrombotic microangiopathies (TMAs), including thrombotic thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS). (biomedcentral.com)
  • An algorithm to rapidly differentiate disseminated intravascular coagulation (DIC) from thrombotic thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS) in the intensive care unit (ICU). (biomedcentral.com)
  • Abnormal coagulation studies, including prothrombin time (PT), activated partial thromboplastin time (aPTT), fibrinogen concentration, fibrin degradation products, D-dimers, and antithrombin, are required for differentiation of DIC from thrombotic microangiopathies (TMAs). (biomedcentral.com)
  • Increased D-dimer concentrations are found in thrombotic diseases and micro thrombotic events (e.g. in case of disseminated intravascular coagulation: DIC). (horiba.com)
  • This in turn results in intravascular formation of fibrin and ultimately thrombotic occlusion of small to medium sized vessels [ 1 ]. (biomedcentral.com)
  • [ 1 ] Consumption and subsequent exhaustion of coagulation proteins and platelets (from ongoing activation of coagulation) may induce severe bleeding, though microclot formation may occur in the absence of severe clotting factor depletion and bleeding. (medscape.com)
  • 0.05 g/L (1.5-4.0), platelets 25 × 10 9 /L (150-400), consistent with disseminated intravascular coagulation (DIC). (biomedcentral.com)
  • Disseminated intravascular coagulation is an acquired acute, subacute or chronic coagulation or thrombohaemorrhagic disorder characterized by formation of microthrombi, consumption of coagulation factors/platelets, activation of fibrinolytic system and haemorrhage. (smjonline.org)
  • Overview of Hemostasis Hemostasis, the arrest of bleeding from an injured blood vessel, requires the combined activity of Vascular factors Platelets Plasma coagulation factors Regulatory mechanisms counterbalance. (merckmanuals.com)
  • Overview of Vascular Bleeding Disorders Bleeding may result from abnormalities in Platelets Coagulation factors Blood vessels Vascular bleeding disorders result from defects in blood vessels, typically causing cutaneous or mucosal. (merckmanuals.com)
  • HAE has a risk of life-threatening complications such as capillary leak syndrome (CLS) and disseminated intravascular coagulation (DIC). (anesth-pain-med.org)
  • therefore many unusual complications of the disease such as Disseminated Intravascular Coagulation would be expected in our hospitals. (smjonline.org)
  • Disseminated intravascular coagulation (DIC) is a serious disorder in which the proteins that control blood clotting become overactive. (medlineplus.gov)
  • Disseminated intravascular coagulation (DIC) is always secondary to some process that leads to pathologic and systemic production of thrombin. (infectiousdiseaseadvisor.com)
  • Abnormalities of blood coagulation parameters are readily identified, and organ failure frequently results. (medscape.com)
  • METHODS--The subjects were 87 patients whose illnesses were complicated by DIC and 64 patients who showed no abnormalities of blood coagulation in their terminal illness. (bmj.com)
  • The subcommittee on DIC of the International Society on Thrombosis and Haemostasis has suggested the following definition for DIC: "An acquired syndrome characterized by the intravascular activation of coagulation with loss of localization arising from different causes. (medscape.com)
  • Disseminated intravascular coagulation (DIC) is really a regular complication in sepsis that's connected with worse outcomes and higher mortality in patients. (bioshockinfinitereleasedate.com)
  • Background This retrospective study was conducted to analyze the temporal trends , predictors, and impact of disseminated intravascular coagulation ( DIC ) on outcomes among septicemic patients using a nationally representative database. (bvsalud.org)
  • Disseminated intravascular coagulation (DIC) is a relatively rare but important cause of bleeding diathesis in patients on maintenance dialysis. (biomedcentral.com)
  • Determine the effects of bevacizumab on coagulation profiles in these patients. (knowcancer.com)
  • How often is heparin-induced thrombocytopenia (HIT) complicated by disseminated intravascular coagulation (DIC)? (thebloodproject.com)
  • His laboratory results showed prolonged coagulation profiles and thrombocytopenia in keeping with Disseminated intravascular coagulation. (smjonline.org)
  • The theoretical mechanism for the coagulation and hemostatic effects of rFVIIa are discussed. (medscape.com)
  • Incidence of pulmonary thromboembolism, infarction and haemorrhage in disseminated intravascular coagulation: a necroscopic analysis. (bmj.com)
  • The aims of this paper are to present a case of Disseminated Intravascular Coagulation complicated by Acute Renal Failure in a patient with underlying pulmonary tuberculosis and also to review the available literature. (smjonline.org)
  • To assess the therapeutic efficacy of agents capable of stimulating the fibrinolytic system, such as tissue plasminogen activator (t-PA) and urokinase (UK) on endotoxin-induced disseminated intravascular coagulation (DIC) in the rabbit. (cun.es)
  • The pathophysiology, diagnosis, and management of sepsis-associated disseminated intravascular coagulation. (qxmd.com)
  • Actually, in situations of sepsis with DIC, liquid resuscitation could possibly be more threatening than helpful since it you could end up myocardial dysfunction or the forming of emboli and consequential infarction of various other vessels.17 Thus, it really is better specifically deal with DIC to be able to mitigate coagulation-associated cells pathogenesis and reduce threat of mortality in sepsis individuals. (bioshockinfinitereleasedate.com)
  • Temporal Trends, Predictors, and Outcomes of Disseminated Intravascular Coagulation in Hospitalizations With Sepsis. (bvsalud.org)
  • DIC is characterised by the widespread activation of coagulation. (biomedcentral.com)
  • Acute DIC develops when sudden exposure of blood to procoagulants (eg, tissue factor [TF], or tissue thromboplastin) generates intravascular coagulation. (medscape.com)
  • Disseminated intravascular coagulation (DIC) is characterized by systemic activation of blood coagulation, which results in generation and deposition of fibrin, leading to microvascular thrombi in various organs and contributing to multiple organ dysfunction syndrome (MODS). (medscape.com)
  • Besides the well-known clinical presentations, HAE may also produce hypovolemic shock due to the tissue leakage of fluids [ 4 ] and may lead to potentially life-threatening conditions such as capillary leak syndrome (CLS) and disseminated intravascular coagulation (DIC) [ 5 , 6 ]. (anesth-pain-med.org)
  • Martius scarlet blue stains indicate presence of fibrin in brain, intestines, kidney and liver, or disseminated intravascular coagulation (DIC). (was.org)
  • Because all coagulation factors are made in the liver (by hepatocytes and hepatic sinusoidal endothelial cells), both the prothrombin time (PT) and partial thromboplastin time (PTT) are prolonged in severe liver disorders. (merckmanuals.com)
  • Disseminated intravascular coagulation (DIC) is a condition in which blood clots form throughout the body, blocking small blood vessels. (wikipedia.org)
  • Disseminated intravascular coagulation (DIC) is a life-threatening condition that prevents a person's blood from clotting normally. (stlukesonline.org)
  • Intravascular means inside the blood vessels. (merckmanuals.com)
  • No doses of t-PA modified the changes appearing in blood coagulation. (cun.es)
  • When micro-thrombi partially block blood flow, red blood cells can be physically sheared as they move past, resulting in an intravascular hemolytic anemia akin to a Microangiopathic Hemolytic Anemia (MAHA). (symptoma.com)
  • The coagulation of blood is maintained by cellular components and soluble plasma proteins. (medscape.com)
  • During plasma coagulation, soluble fibrin is generated by the influence of thrombin on fibrinogen. (horiba.com)
  • This policy review addresses whether early hemorrhagic smallpox is disseminated intravascular coagulation and speculates about the cause of the high mortality rate among pregnant women and whether ocular smallpox is partly the result of trachoma or vitamin A deficiency. (cdc.gov)
  • Advanced gastric cancer (AGC) rarely presents with disseminated intravascular coagulation (DIC) at the time of diagnosis before treatment with no current standard chemotherapy (CTx) regimen. (nih.gov)
  • TF has been demonstrated to exist in normal vascular endothelial cells suggesting a role in initiating rapid activation of coagulation. (biomedcentral.com)
  • Coagulation entails sequential activation of some plasma proteases converging around the era UK-427857 of triggered thrombin. (bioshockinfinitereleasedate.com)
  • Significantly, the activation of coagulation also feeds back again onto the immune system response. (bioshockinfinitereleasedate.com)
  • Serine proteases, such as for example thrombin, have the ability to cleave substances referred to as protease-activated receptors (PARs) and latest work shows a clear part for PAR activation in sponsor immunity.18, 19 This crossover between coagulation and immunity highlights the necessity for strategies that modulate, however, not completely inhibit immune-mediated coagulation. (bioshockinfinitereleasedate.com)
  • BACKGROUND--The pathological features of the lung in disseminated intravascular coagulation (DIC) have not been established. (bmj.com)
  • Septic shock, multiple organ failure, and disseminated intravascular coagulation. (qxmd.com)
  • Disseminated Intravascular Coagulation (DIC) complicates up to 7% of malignancies, the commonest solid organ association being adenocarcinoma. (biomedcentral.com)
  • This complex further activates factor IX and X to IXa and Xa, respectively, leading to the common coagulation pathway and the subsequent formation of thrombin and fibrin. (wikipedia.org)
  • In a postoperative patient, there is bleeding from all incisions, wounds, and at insertion sites of intravascular devices. (infectiousdiseaseadvisor.com)
  • This disease had all the hallmarks of disseminated intravascular coagulation (DIC). (cdc.gov)
  • Coagulation factor complex. (empr.com)
  • Not for treating bleeding episodes due to coagulation factor deficiencies in the absence of inhibitors to factor VIII or IX. (empr.com)