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    Blood Physiology Part 2 Dr. Olivar

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    Jorelyn Frias
    Hemostasis is achieved through vasoconstriction, platelet plug formation, and blood coagulation. Platelets play a key role in hemostasis by forming a platelet plug to seal defects in blood vessels. When a blood vessel is injured, platelets are attracted to the exposed collagen and form a platelet plug to prevent blood loss. If the platelet plug is insufficient, the blood coagulation cascade is activated through intrinsic and extrinsic pathways ultimately resulting in a cross-linked fibrin clot stabilized by Factor XIII to stop bleeding. The clot then retracts and is dissolved through fibrinolysis to complete hemostasis and repair of the blood vessel wall.

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    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd

    Blood Physiology Part 2 Dr. Olivar

    Uploaded by

    Jorelyn Frias
    118 views5 pages
    Hemostasis is achieved through vasoconstriction, platelet plug formation, and blood coagulation. Platelets play a key role in hemostasis by forming a platelet plug to seal defects in blood vessels. When a blood vessel is injured, platelets are attracted to the exposed collagen and form a platelet plug to prevent blood loss. If the platelet plug is insufficient, the blood coagulation cascade is activated through intrinsic and extrinsic pathways ultimately resulting in a cross-linked fibrin clot stabilized by Factor XIII to stop bleeding. The clot then retracts and is dissolved through fibrinolysis to complete hemostasis and repair of the blood vessel wall.

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    Blood Physiology Part 2

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    6. Blood Physiology Part 2 Dr. Olivar

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    Hemostasis is achieved through vasoconstriction, platelet plug formation, and blood coagulation. Platelets play a key role in hemostasis by forming a platelet plug to seal defects in blood vessels. When a blood vessel is injured, platelets are attracted to the exposed collagen and form a platelet plug to prevent blood loss. If the platelet plug is insufficient, the blood coagulation cascade is activated through intrinsic and extrinsic pathways ultimately resulting in a cross-linked fibrin clot stabilized by Factor XIII to stop bleeding. The clot then retracts and is dissolved through fibrinolysis to complete hemostasis and repair of the blood vessel wall.

    Copyright:

    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd
    Download as pdf or txt
    118 views5 pages

    Blood Physiology Part 2 Dr. Olivar

    Uploaded by

    Jorelyn Frias
    Hemostasis is achieved through vasoconstriction, platelet plug formation, and blood coagulation. Platelets play a key role in hemostasis by forming a platelet plug to seal defects in blood vessels. When a blood vessel is injured, platelets are attracted to the exposed collagen and form a platelet plug to prevent blood loss. If the platelet plug is insufficient, the blood coagulation cascade is activated through intrinsic and extrinsic pathways ultimately resulting in a cross-linked fibrin clot stabilized by Factor XIII to stop bleeding. The clot then retracts and is dissolved through fibrinolysis to complete hemostasis and repair of the blood vessel wall.

    Copyright:

    © All Rights Reserved
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    of 5

    Far Eastern University

    Nicanor Reyes Medical Foundation


    Institute of Medicine
    1D Batch 2020 Response to Vessel Trauma/injury
    **HEMOSTASIS IS ACHIEVED
    THROUGH THESE ACTIONS**
    Physiology A - Blood Physiology (Part 2)
    Dr. Joseph U. Olivar 1. Vasoconstriction
    1st line of defense
    Platelets Lowers the blood flow so
    Thrombocytes less platelets will go out
    Small, colorless, non-nucleated Local response from the
    Comes from a single pluripotent smooth muscle
    hematopoietic stem cells 2. Platelet Plug
    Myeloid progenitor cells 2nd line of defense
    Megakaryocytes Whenever the vessel wall
    is exposed (collagen),
    Megakaryocytes platelets are attracted to
    Large cells in the bone marrow the area to seal the
    Before they go out, they fragment defects
    into smaller pieces until they Quite important because
    become platelets many blood vessels
    raptured daily
    Thrombocytopenia Platelets are less
    Poor quality of platelets
    than the normal value; a tendency to
    will result to petechiae
    bleed
    (small red marks) &
    purpura (big red marks)
    Thrombocytosis Platelets are greater
    hemorrhages
    than the normal value; a tendency for
    3. Blood Coagulation
    clotting
    3rd line of defense
    Follows the platelet
    Functions of Platelets:
    plugging if it is not enough
    to stop the bleeding
    1. To achieve HEMOSTASIS, thus
    to stop the bleeding BLOOD CLOTTING OCCURS IN 3
    2. When collagen is exposed, the ESSENTIAL STEPS
    platelets are attracted there thus
    forming the Platelet Plug; 1. Formation of the Prothrombin
    preventing the blood from coming Activator/Prothrombin Converting
    out of the vessel Enzyme - RATE LIMITING STEP
    3. Important for blood coagulation Prothrombin Activator is the
    4. Assists in the vasoconstriction by rate limiting enzyme
    releasing THROMBOXANE A2 2. Conversion of Prothrombin to
    and SEROTONIN Thrombin
    5. Cause the clot to retract by the 3. Conversion of Fibrinogen to Fibrin
    substance released by the
    platelet - thrombosthenin *FIBRIN IS AN UNSTABLE CLOT
    BECAUSE IT IS JUST A
    MONOMER**

    Escoto,KC//Gloriani,KP
    1 of 5
    It should be polymerized *ONCE A SMALL LETTER a IS
    Factor XIII is responsible for WRITTEN AFTER THE ROMAN
    the polymerization *if FXIII is NUMERAL, IT IS ALREADY
    lacking, the person continues ACTIVATED*
    to bleed*
    INITIATION OF BLOOD CLOTTING
    CLOT activates the rate limiting steps
    it is the fibrin itself of clotting
    Stops the bleeding of the blood 1. Trauma to the vascular wall and
    vessel adjacent cells (Extrinsic)
    a STABLE CLOT is composed of 2. Contact of blood with damaged
    fibrin polymers, platelets, RBC and endothelial cells (Intrinsic)
    most of the Coagulation Factors 3. Trauma to the blood (Intrinsic)
    HEMATOMA
    Rupture of vessel with intact skin
    so the blood forms under the skin
    COAGULATION FACTORS exists in
    the plasma (pro-coagulant/non-active)

    FACTOR SYNONYMS
    Factor I Fibrinogen
    Factor II Prothrombin
    Factor III Tissue Factor /
    Thromboplastin
    Factor IV Calcium Ion
    Factor V Labile Factor /
    Proaccelerin
    Factor VII Stable Factor /
    Proconvertin
    Factor VIII Antihemophilic Common Pathway (the prothrombin
    Factor A converting enzyme is found here in the
    Factor IX Antihemophilic B/ activation of FX)
    Christmas factor FACTOR X FXa [prothrombin
    Factor X Stuart Prower activator] that converts
    Factor prothrombin to thrombin
    Factor XI Antihemophilic C/ Thrombin converts fibrinogen to
    Plasma fibrin
    Thromboplastin Fibrin is stabilized by Factor XIII
    Antecedent to produce a stable clot
    Factor XII Hageman factor
    Factor XIII Fibrinogen Extrinsic Pathway
    Stabilizing Factor Caused by tissue trauma
    High Molecular Fitzgerald factor Shorter and rapid
    Weight Kininogen ONLY 2 FACTORS: FIII and FVII
    Prekallikrein Fletcher factor

    Escoto,KC//Gloriani,KP
    2 of 5
    Involves the release of Factor III 1. Blue top/citrate deionizes
    that immediately activates Factor calcium
    VII 2. Gray top/oxalate precipitates
    The Combination of FIII and calcium
    FVII automatically converts FX
    FXa CLOT RETRACTION
    Going to common pathway After sometime in coagulation,
    the clot will retract, forming the
    Intrinsic Pathway serum
    Begins with the FXII FXIIa As the clot retracts, the edges of
    FXI FXIa the broken blood vessels are
    FIX FIXa that combines with pulled together (approximation),
    FVIII that activates FX to Xa contributing to the ULTIMATE
    Going to common Pathway STATE OF HEMOSTASIS
    Plasma formed when blood is
    *some people lack Factor VIII placed in an anticoagulation tube;
    (HEMOPHILIA) so the person contains coagulation factors
    continues bleeding because
    when nothing combines with FIX, Serum formed when blood is
    FX is not activated placed in a tube that allows
    coagulation; no coagulation factors is
    present in the serum because they are
    all present in the clotted blood
    Liquid portion of the clotted blood

    THE FINAL STATE OF HEMOSTASIS


    DICTATES THAT THE BLOOD
    VESSEL SHOULD REPAIR ITSELF.
    *happens only when the edges are
    approximated brought about by the clot
    retraction*

    LYSIS OF THE CLOT


    The clot will have no function
    after the retraction so it needs to
    be dissolved
    **CALCIUM, PHOSPHOLIPIDS & Fibrinolysis or lysis of clot is a
    PLATELETS ARE ALWAYS INVOLVE function of PLASMIN
    even the coagulation factors are
    present/adequate, without the three,
    there will be NO CLOT FORMATION** PLASMIN
    Removes the clot from the
    ANTICOAGULANTS emphasizes vessels that eventually become
    the role of calcium in the clot occluded where there is no way
    formation to clean them

    Escoto,KC//Gloriani,KP
    3 of 5
    Fibrinolytic Pathway **FIBRIN IS A NATURAL
    ANTICOAGULANT THAT HAS
    ANTITHROMBIN ACTION**

    Clinical Correlations Coagulation


    disorders

    Deficiency in coagulation bleeding


    Vitamin K is important in the
    activation of several coagulation
    factors [Factors IX, X, VII & II]
    {9,10,7,2} which are produced by
    the liver and activated by liver
    carboxylase
    Vit. K is synthesized by
    INTESTINAL FLORA/bacteria
    Vitamin K needs fat and bile to be
    absorbed by the liver. [The bile
    Streptokinase/Urokinase Drugs that produced in the liver emulsifies
    are analog to tissue plasminogen the fat.]
    activator (tPA) which accelerates the Once activated, it become
    conversion of plasminogen to plasmin. reduced
    Fibrinolytic agent lyses the clot VCOR C1 reactivates the
    Tranexamic acid anti-fibrinolytic reduced form of Vitamin K
    agent that prolongs the stay of the clot
    Vitamin K deficiency happens when
    INTRAVASCULAR the common bile duct is cut or
    ANTICOAGULANTS disconnected from the duodenum to the
    Glycocalyx & Thrombomodulin liver; also happens in newborn because
    Prevents blood clotting when their intestine is sterile
    there is no injury or trauma Hemophilia lack of Factor VIII
    Excess in coagulation abnormal
    Intravascular Anticoagulants: clotting
    Glycocalyx a negatively charged Formation of unnecessary clots
    protein that lines the SMOOTH blood Thrombus
    vessels and repels the coagulation Abnormal clot formation
    factors that try to attached to it [only for Embolus
    smooth lining. In ATHEROSCLEROSIS, A thrombus that is thrown
    the glycocalyx is lost] into circulation and causes
    infarction
    Thrombomodulin protein that can Usually formed in the deep
    bind thrombin and INHIBITS it to form veins of the lower
    PROTEIN C extremities
    Lodges in the pulmonary
    PROTEIN C inactivates Factor V & capillaries due to small
    Factor VIII

    Escoto,KC//Gloriani,KP
    4 of 5
    diameters of the arteries Anticoagulants
    there
    Clots that will lodge on the 1. Heparin
    left pulmonary capillaries Combines with anti-
    came from the left side thrombin 3 to become a
    [due to abnormal pumping powerful anticoagulant
    of the heart, forming clots Antidote: Protamine
    in the mitral valve and Sulfate
    thrown up to the cerebral
    arteries that commonly 2. Coumadin/Warfarin
    cause stroke] Inhibits/block Vitamin K
    epoxide reductase
    Atherosclerosis [VCORC1] so there will be
    Buildup of cholesterol in no production of Factors
    the tunica intima IX, X, VII & II
    Diameter of the vessel Antidote: Vitamin K
    decreases and will make
    the person hypertensive Bleeding time
    High blood pressure can - Test for platelet quality
    damage the endothelial Clotting time
    tissue, exposing the - Test for clotting factors
    collagen and activating the o Prothrombin Time (PT)
    intrinsic pathway of Test for EXTRINSIC
    clotting. As the clot gets PATHWAY
    bigger it will clog the small * Mnemonics: PeT
    diameter vessel causing a
    heart attack / myocardial o Partial Thromboplastin
    infarction Time (PTT)
    Test for INTRINSIC
    Disseminated Intravascular PATHWAY
    Coagulation
    All the coagulation factors
    are consoled causing
    widespread clotting
    Also known as
    Consumptive
    Coagulopathy
    ENDPOINT: BLEEDING
    Removal of the cause is
    the treatment

    Ive got to find my way, and I will


    survive some way.
    -Tarzan
    Escoto,KC//Gloriani,KP
    5 of 5

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