Coagulation studies are a group of hematologic laboratory studies that reflect the function of blood vessels, platelets Platelets Platelets are small cell fragments involved in hemostasis. Thrombopoiesis takes place primarily in the bone marrow through a series of cell differentiation and is influenced by several cytokines. Platelets are formed after fragmentation of the megakaryocyte cytoplasm. Platelets: Histology, and coagulation factors Coagulation factors Endogenous substances, usually proteins, that are involved in the blood coagulation process. Hemostasis, which all interact with one another to achieve hemostasis Hemostasis Hemostasis refers to the innate, stepwise body processes that occur following vessel injury, resulting in clot formation and cessation of bleeding. Hemostasis occurs in 2 phases, namely, primary and secondary. Primary hemostasis involves forming a plug that stops the bleeding temporarily. Secondary hemostasis involves the activation of the coagulation cascade. Hemostasis. Coagulation studies are usually ordered to evaluate patients Patients Individuals participating in the health care system for the purpose of receiving therapeutic, diagnostic, or preventive procedures. Clinician–Patient Relationship with bleeding or hypercoagulation disorders.
Last updated: 8 Apr, 2021
Coagulation studies are a group of hematologic studies that reflect the function of blood vessels, platelets Platelets Platelets are small cell fragments involved in hemostasis. Thrombopoiesis takes place primarily in the bone marrow through a series of cell differentiation and is influenced by several cytokines. Platelets are formed after fragmentation of the megakaryocyte cytoplasm. Platelets: Histology, and coagulation factors Coagulation factors Endogenous substances, usually proteins, that are involved in the blood coagulation process. Hemostasis, which all work in harmony to achieve hemostasis Hemostasis Hemostasis refers to the innate, stepwise body processes that occur following vessel injury, resulting in clot formation and cessation of bleeding. Hemostasis occurs in 2 phases, namely, primary and secondary. Primary hemostasis involves forming a plug that stops the bleeding temporarily. Secondary hemostasis involves the activation of the coagulation cascade. Hemostasis.
The following is a summary of the hemostatic process:
Formation of the temporary hemostatic plug:
The disrupted endothelial surface exposes
von Willebrand Factor
von Willebrand factor
A high-molecular-weight plasma protein, produced by endothelial cells and megakaryocytes, that is part of the factor VIII/von Willebrand factor complex. The von Willebrand factor has receptors for collagen, platelets, and ristocetin activity as well as the immunologically distinct antigenic determinants. It functions in adhesion of platelets to collagen and hemostatic plug formation. The prolonged bleeding time in von Willebrand diseases is due to the deficiency of this factor.
Hemostasis (vWF) to the passing blood.
Platelets
Platelets
Platelets are small cell fragments involved in hemostasis. Thrombopoiesis takes place primarily in the bone marrow through a series of cell differentiation and is influenced by several cytokines. Platelets are formed after fragmentation of the megakaryocyte cytoplasm.
Platelets: Histology
bind
BIND
Hyperbilirubinemia of the Newborn to the vWF via their GpIb
receptors
Receptors
Receptors are proteins located either on the surface of or within a cell that can bind to signaling molecules known as ligands (e.g., hormones) and cause some type of response within the cell.
Receptors and are activated.
Platelet activation
Platelet activation
A series of progressive, overlapping events, triggered by exposure of the platelets to subendothelial tissue. These events include shape change, adhesiveness, aggregation, and release reactions. When carried through to completion, these events lead to the formation of a stable hemostatic plug.
Hemostasis
triggers
Triggers
Hereditary Angioedema (C1 Esterase Inhibitor Deficiency) them to secrete
adenosine
Adenosine
A nucleoside that is composed of adenine and d-ribose. Adenosine or adenosine derivatives play many important biological roles in addition to being components of DNA and RNA. Adenosine itself is a neurotransmitter.
Class 5 Antiarrhythmic Drugs diphosphate (ADP), which stimulates the expression of the GpIIb/IIIa
receptors
Receptors
Receptors are proteins located either on the surface of or within a cell that can bind to signaling molecules known as ligands (e.g., hormones) and cause some type of response within the cell.
Receptors on the
platelets
Platelets
Platelets are small cell fragments involved in hemostasis. Thrombopoiesis takes place primarily in the bone marrow through a series of cell differentiation and is influenced by several cytokines. Platelets are formed after fragmentation of the megakaryocyte cytoplasm.
Platelets: Histology. The GpIIb/IIIa
receptors
Receptors
Receptors are proteins located either on the surface of or within a cell that can bind to signaling molecules known as ligands (e.g., hormones) and cause some type of response within the cell.
Receptors
bind
BIND
Hyperbilirubinemia of the Newborn to
fibrinogen
Fibrinogen
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.
Hemostasis, which is able to
bind
BIND
Hyperbilirubinemia of the Newborn a platelet on each end, causing
platelets
Platelets
Platelets are small cell fragments involved in hemostasis. Thrombopoiesis takes place primarily in the bone marrow through a series of cell differentiation and is influenced by several cytokines. Platelets are formed after fragmentation of the megakaryocyte cytoplasm.
Platelets: Histology to aggregate. As more
platelets
Platelets
Platelets are small cell fragments involved in hemostasis. Thrombopoiesis takes place primarily in the bone marrow through a series of cell differentiation and is influenced by several cytokines. Platelets are formed after fragmentation of the megakaryocyte cytoplasm.
Platelets: Histology are bound to one another, the
platelet plug
Platelet plug
Hemostasis is generated. As the
coagulation cascade
Coagulation cascade
The coagulation cascade is a series of reactions that ultimately generates a strong, cross-linked fibrin clot.
Hemostasis is activated,
thrombin
Thrombin
An enzyme formed from prothrombin that converts fibrinogen to fibrin.
Hemostasis converts the weaker
fibrinogen
Fibrinogen
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.
Hemostasis into the stronger
fibrin
Fibrin
A protein derived from fibrinogen in the presence of thrombin, which forms part of the blood clot.
Rapidly Progressive Glomerulonephritis, creating a much more stable clot.
Overview of the
coagulation cascade
Coagulation cascade
The coagulation cascade is a series of reactions that ultimately generates a strong, cross-linked fibrin clot.
Hemostasis
a: activated form
PF3: platelet factor 3 (
phospholipids
Phospholipids
Lipids containing one or more phosphate groups, particularly those derived from either glycerol (phosphoglycerides) or sphingosine (sphingolipids). They are polar lipids that are of great importance for the structure and function of cell membranes and are the most abundant of membrane lipids, although not stored in large amounts in the system.
Lipid Metabolism)
The following studies can assist in diagnosing issues related to hemostasis Hemostasis Hemostasis refers to the innate, stepwise body processes that occur following vessel injury, resulting in clot formation and cessation of bleeding. Hemostasis occurs in 2 phases, namely, primary and secondary. Primary hemostasis involves forming a plug that stops the bleeding temporarily. Secondary hemostasis involves the activation of the coagulation cascade. Hemostasis.
Platelet counts:
Bleeding time Bleeding time Duration of blood flow after skin puncture. This test is used as a measure of capillary and platelet function. Hemostasis (BT):
These studies are used to assess the amount of time it takes plasma Plasma The residual portion of blood that is left after removal of blood cells by centrifugation without prior blood coagulation. Transfusion Products to clot when various substances are added.
Assessing the coagulation cascade Coagulation cascade The coagulation cascade is a series of reactions that ultimately generates a strong, cross-linked fibrin clot. Hemostasis
Image by Lecturio.Coagulation factor assays primarily used to diagnose specific factor deficiencies. The tests are used to assess the concentration or activity level of individual factors.
Mixing studies are used to further evaluate an unexplained prolongation of a clotting test, including a prolonged PT, aPTT, or TT.
Hypocoagulable Hypocoagulable Hypocoagulable conditions, also known as bleeding disorders or bleeding diathesis, are a diverse group of diseases that result in abnormal hemostasis. Physiologic hemostasis is dependent on the integrity of endothelial cells, subendothelial matrix, platelets, and coagulation factors. The hypocoagulable states result from abnormalities in one or more of these contributors, resulting in ineffective thrombosis and bleeding. Hypocoagulable Conditions conditions are a group of diseases that result in abnormal hemostasis Hemostasis Hemostasis refers to the innate, stepwise body processes that occur following vessel injury, resulting in clot formation and cessation of bleeding. Hemostasis occurs in 2 phases, namely, primary and secondary. Primary hemostasis involves forming a plug that stops the bleeding temporarily. Secondary hemostasis involves the activation of the coagulation cascade. Hemostasis. They manifest with minor bleeding ( petechiae Petechiae Primary Skin Lesions, mucocutaneous bleeding) or more severe internal bleeding ( hemarthrosis Hemarthrosis Bleeding into the joints. It may arise from trauma or spontaneously in patients with hemophilia. Hemophilia, intracranial bleeding).
Patients Patients Individuals participating in the health care system for the purpose of receiving therapeutic, diagnostic, or preventive procedures. Clinician–Patient Relationship with these disorders will most likely have an increased bleeding time Bleeding time Duration of blood flow after skin puncture. This test is used as a measure of capillary and platelet function. Hemostasis but normal PT and aPTT.
Hemophilia Hemophilia The hemophilias are a group of inherited, or sometimes acquired, disorders of secondary hemostasis due to deficiency of specific clotting factors. Hemophilia A is a deficiency of factor VIII, hemophilia B a deficiency of factor IX, and hemophilia C a deficiency of factor XI. Patients present with bleeding events that may be spontaneous or associated with minor or major trauma. Hemophilia: a rare blood clotting disorder in which the body lacks blood-clotting factors ( factor VIII Factor VIII Factor VIII of blood coagulation. 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. Hemostasis in hemophilia A Hemophilia A The classic hemophilia resulting from a deficiency of factor VIII. It is an inherited disorder of blood coagulation characterized by a permanent tendency to hemorrhage. Hemophilia and factor IX Factor IX Storage-stable blood coagulation factor acting in the intrinsic pathway of blood coagulation. Its activated form, ixa, forms a complex with factor VIII and calcium on platelet factor 3 to activate factor X to Xa. Hemostasis in hemophilia B Hemophilia B A deficiency of blood coagulation factor IX inherited as an X-linked disorder. (also known as Christmas disease, after the first patient studied in detail, not the holiday.) historical and clinical features resemble those in classic hemophilia, but patients present with fewer symptoms. Severity of bleeding is usually similar in members of a single family. Many patients are asymptomatic until the hemostatic system is stressed by surgery or trauma. Treatment is similar to that for hemophilia A. Hemophilia). Affected individuals present with abnormal bleeding that occurred spontaneously or after minor trauma. Patients Patients Individuals participating in the health care system for the purpose of receiving therapeutic, diagnostic, or preventive procedures. Clinician–Patient Relationship can bleed into joint spaces and can develop life-threatening internal bleeding. Coagulation studies typically reveal a prolonged aPTT due to the abnormalities in the intrinsic pathway Intrinsic pathway The intrinsic pathway is mainly responsible for the amplification of factor X activation Hemostasis, but the PT and platelet counts are normal. Mixing studies will correct, and the level of the specific factor activity in which the patient is deficient will be low.