Please enable JavaScript.

Coggle requires JavaScript to display documents.

PATHO 3: DISORDER OF CVS - Coggle Diagram

- - - - PHASE
        
        VASCULAR
        
        VASCULAR SPASM
        
        Vasoconstriction is the narrowing of the blood vessels, which increases blood pressure but can decrease blood flow and loss.
        ● Vasoconstriction is mediated by contraction of the smooth muscles lining a blood vessel.
        ● Vasoconstriction is caused by thromboxane A2 from activated platelets and injured epithelial cells, nervous system reflexes from pain, and direct injury to vascular smooth muscle.
        ● Vasonstriction only lasts for a few minutes during hemostasis. During inflammation that follows the injury, it is replaced by vasodilation as the healing process begins.
        
        VASOCONSTRICTION
        
        MECH?
        
        The vasoconstriction response is triggered by factors such as a direct injury to vascular smooth muscle, signaling molecules released by injured endothelial cells and activated platelets (such as thromboxane A2), and nervous system reflexes initiated by local pain receptors.
        ● The spasm response becomes more effective as the amount of damage is increased.
        ● Vascular spasm is much more effective at slowing the flow of blood in smaller blood vessels.
        ● Vasoconstriction also causes an increase in blood pressure for affected blood vessels.
        
        Smooth muscle in the vessel wall goes through intense contractions that constrict the vessel.
        ● If the vessels are small, spasms compress the inner walls together and may be able to stop the bleeding completely.
        ● If the vessels are medium to large-sized, the spasms slow down immediate outflow of blood, lessening the damage but still preparing the vessel for the later steps of hemostasis.
        ● The spasm response becomes stronger and lasts longer in more severe injuries.
        ● Vasoconstriction may be induced by drugs called vasopressins, which increase blood pressure and can help treat certain conditions.
        
        During injury & inflammation..
        
        Vasoconstriction is brief, lasting only a few minutes while the platelet plug and coagulation cascade occur.
        
        ● During the process,
        i) inflammatory mediator release from immune system cells (such as mast cells or NK cells) that receive cell stress cytokines from damaged endothelial cells or
        ii) vasoactive amines (serotonin) that are secreted by activated platelets.
        ● During inflammation, vasodilation occur, along with increased vascular permeability and leukocyte chemotaxis, ending the spasm of vasoconstriction and hemostasis as wound healing begins.
        
        PLATELET
        
        FXN:
        
        Platelet
        adherence
        
        Normally, the endothelial cells express molecules that inhibit platelet adherence and activation while platelets circulate through the blood vessels.
        ● These molecules include nitric oxide, prostacylcine (PGI2) and endothelial ADP-ase.
        ● During an injury, subendothelial collagen from the extracellular matrix beneath the endothelial cells is exposed on the epithelium as the normal epithelial cells are damaged and removed, which releases von Willebrand Factor (VWF).
        ● VWF causes the platelets to change form with adhesive filaments (extensions) that adhere to the subendothelial collagen on the endothelial wall.
        
        After platelet adherence occurs, the subendothelial collagen binds to receptors on the platelet, which activates it.
        ● During platelet activation, the platelet releases a number of important cytokines and chemical mediators via degranulation
        
        CYTOKINE & MEDIATOR
        
        7 more items...
        
        Platelet
        aggregation
        
        The final step of platelet plug formation is aggregation of the platelets into a barrier-like plug.
        ● Receptors on the platelet bind to VWF and fibrinogen molecules, which hold the platelets together.
        ● Platelets may also bind to subendothelial VWF to anchor them to the damaged endothelium.
        ● The completed plug will cover the damaged components of the endothelium and will stop blood from flowing out of it.
        ● If the wound is large enough, blood will not coagulate until the fibrin mesh from the coagulation cascade is produced, which strengthens the platelet plug.
        ● If the wound is minor, the platelet plug may be enough to stop the bleeding without the coagulation cascade.
        
        What)make)platelet)remain)
        inactive)in)healthy)vessel?
        
        3 more items...
        
        Provide surface attachment for coagulation factors
        
        Prothrombin --> thrombin --> fibrinogen --> fibrin --> fibrin mesh
        
        COAGULATIVE
        
        Coagulation is the process by which a blood clot forms to reduce blood loss after damage to a blood vessel.
        • Several components of the coagulation cascade, including both cellular (e.g. platelets) and protein (e.g. fibrin) components, are involved in blood vessel repair.
        • The role of the cellular and protein components can be categorized as primary hemostasis (the platelet plug) and secondary hemostasis (the coagulation cascade).
        
        The coagulation cascade is a series of reactions, which is classically divided into three pathways: the contact (intrinsic) pathway, the tissue factor (extrinsic pathway), and the common pathway.
        • The intrinsic pathway occurs when negatively charged molecule contact causes a cascade of factors that produce factor X.
        • The extrinsic pathway occurs when tissue damage causes the release of tissue factor, creating a smaller cascade that produces factor X.
        • The common pathway merges both pathways as factor X is used to activate prothrombin ! thrombin.
        
        EXTRINSIC
        
        The quicker responding and more direct extrinsic begins when damage occurs to the surrounding tissues, such as in a traumatic injury.
        ● Upon contact with blood plasma, the damaged extravascular cells, which are extrinsic to the bloodstream, release factor III (thromboplastin).
        ● Sequentially, Ca2+ then factor VII (proconvertin), which is activated by factor III, are added, forming an enzyme complex.
        ● This enzyme complex leads to activation of factor X (Stuart–Prower factor), which activates the common pathway.
        ● The events in the extrinsic pathway are completed in a matter of seconds.
        
        INTRINSIC
        
        The intrinsic pathway is longer and more complex.
        ● In this case, the factors involved are intrinsic to (present within) the bloodstream.
        ● The pathway can be prompted by damage to the tissues, resulting from internal factors such as arterial disease;
        ● however, it is most often initiated when factor XII (Hageman factor) comes into contact with foreign materials, such as when a blood sample is put into a glass test tube.
        ● Within the body, factor XII is typically activated when it encounters negatively charged molecules, such as inorganic polymers and phosphate produced earlier in the series of intrinsic pathway reactions.
        ● Factor XII sets off a series of reactions that in turn activates factor XI (antihemolytic factor C or plasma thromboplastin antecedent) then factor IX (antihemolytic factor B or plasma thromboplasmin).
        ● Finally, factor VIII (antihemolytic factor A) from the platelets and endothelial cells combines with factor IX (antihemolytic factor B or plasma thromboplasmin) to form an enzyme complex that activates factor X (Stuart–Prower factor or thrombokinase), leading to the common pathway.
        ● The events in the intrinsic pathway are completed in a few minutes.
        
        COMMON
        
        In the final common pathway, prothrombin (Factor II) is converted to thrombin.
        ● When factor X is activated by either the intrinsic or extrinsic pathways, it activates prothrombin (also called factor II) and converts it into thrombin using factor V.
        ● Thrombin then cleaves fibrinogen into fibrin, which forms the mesh that binds to and strengthens the platelet plug, finishing coagulation and thus hemostasis.
        ● It also activates more factor V, which later acts as an anticoagulant with inhibitor protein C, and factor XIII, which covalently bonds to fibrin to strengthen its attachment to the platelets.
        
        Secondary hemostasis involves factors of the coagulation cascade, which collectively strengthen the platelet plug.
        • Coagulation can be harmful if blood clots embolize and obstruct other blood vessels. Clots can also occur if blood pools from prolonged immobility.
        • A number of anticoagulants exist to inhibit various parts of the coagulation cascade, inactivate thrombin, or degrade fibrin directly.
        
        FIBIRINOLYTIC
        
        Process the remove clots after hemostasis and clot retraction --> prevent thrombosis and embolism
        
        2 TYPES
        
        Primary fibrinolysis
        
        Primary fibrinolysis normally occurs following clot retraction, in which the clot has already condensed considerably in size.
        ● The main enzyme in primary fibrinolysis is plasmin, (function= proteolytic enzyme that degrades fibrin mesh).
        ● Plasmin cleaves fibrin at various places, leading to the production of circulating fragments that are cleared by other proteases or by the kidneys and liver.
        ● Plasmin is produced in an inactive form, plasminogen, in the liver.
        ● Plasminogen cannot cleave fibrin and circulates in the bloodstream. Instead, it is incorporated into the clot when it is formed and then activated into plasmin later.
        ● Plasminogen is activated to plasmin by tissue plasminogen activator (t-PA) and urokinase, an enzyme found in the urine.
        
        T-PA is released into the blood very slowly by the damaged endothelium of the blood vessels.
        ● T-PA and urokinase are themselves inhibited by plasminogen activator inhibitor-1 and plasminogen activator inhibitor-2 (PAI-1 and PAI-2).
        ● In contrast, plasmin further stimulates plasmin generation by producing more active forms of both tissue plasminogen activator (tPA) and urokinase.
        ● Following fibrin degradation by plasmin, old activated platelets from the platelet plug are phagocytized and destroyed by macrophages.
        
        1 more item...
        
        Secondary fibrinolysis