Blood 2 A&P II Lecture

  1. Coagulation Phase 1: Two Pathways to Prothrombin Activator
    Ititiated by either the intrinsic or extrinsic pathway (usually both)

    • -triggered by tissue-damaging events
    • -involves a series of pro-coagulents
    • -each pathways cascades towards factor X

    Factor X complexes with Ca2+, PF3, and factor V to form prothrombin activator

    *phase 1 is the slowest part. once prothrombin actovator is formed, clot is created in 10-15 seconds*
  2. Describe the 2 Pathways to Prothrombin Activator during Phase 1 of Coagulation
    • Intrinsic Pathway:
    • -is triggered by nefatively charged surfaces (Activated platelets, collagen, glass)
    • -Uses factors present within the blood (intrinsic)

    • Extrinsic Pathway:
    • -Is triggered by exposure to tissue factor (TF) or factor III (an extrinsic factor)
    • -by passes several steps of the intrinsic pathway, so it is faster
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  3. Explain Coagulation Phase 2: Pathway to Thrombin
    • Prothrombin activator catalyzes the transformation of prothrombin to the active enzyme thrombin
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  4. Explain Coagulation Phase 3: Common pathway to fibrin mesh
    Thrombin converts the soluable fribrinogen into fibrin

    fibrin strands form the structural basis of a clot

    Fibrin causes plasma to become a gel-like trap for formed elements

    • Thrombin (with Ca2+) activates factor VIII which:
    • -cross links fibrin
    • -strengthens and stabilizes the clot until it can become permanently repairs
  5. Explain Clot Retraction and Clot repair
    • Clot retraction:
    • -Actin and Myosin in platelets contract within 30-60 minutes
    • -Platelets pull on fibrin strands, squeezing out serum from the clot 

    • Clot repair:
    • -platelet derived growth factor (PDGF) stimulates division of smooth muscle cells and fibroblasts to rebuild blood vessel wall
    • -Vascular endothelial growth factor (VEGF) stimulates endothelial cells toe multiply and restore the endothelial lining
  6. Describe Fibrinolysis
    Keeps clots from growing and getting out of control

    Plasminogen in clot is converted into plasmin by tissue plasminogen actovator (tPA), factor XII, and thrombin

    Plasmin is a fibrin-digesting enzyme
  7. Name the two homeostatic mechanisms that prevent clots from becoming large
    1. Swift removal and dillution of clotting factors

    2. Inhibition of activated clotting factors
  8. How are clotting factors inhibited?
    Most thrombin is bound to fibrin threads, preventing it from acting elsewhere

    Antithrombin III, protein C, and heparin inactivate thrombin and other procoagulents

    Hepain, another anticoagulent, also inhibits thrombin activity
  9. What are the factors preventing undesireable clotting?
    • Platelet adhesion is prevented by
    • -smooth endothelial lining of blood vessels
    • -antithrombic substances, NO, annd prostacylin secreted by endothelial cells
    • -Vitamin E quinine (VitE plus O2) acts as potent anticoagulent
  10. Name two kinds of disorders the interfere with Hemostasis
    Thromboembolytic disorders: undesireable clot formation

    Bleeding Disorders: abnormalities that prevent clot formation
  11. Name 2 Thromboembolytic Conditons and how they are prevented
    • Thrombus: clot that develops and persists in an unbroken blood vessel
    • -may block circulation, leading to tissue deat (like a heart attack)

    • Embolus: a thrombus freely floating in the blood stream
    • -pulmonary emboli impair the ability of the body to obtain O2
    • -cerebral emboli can cause strokes

    • Prevented by:
    • -Asprin: antiprostaglandin that inhibits thromboxane A2
    • -Hepatin: anticoagulent used clinically for pre and post operatice cardiac care
    • -Warfarin (Coumadin)-used for those prone to A-fib
  12. What is DIC?
    Disseminated Intravascular Coagulation (DIC)

    Widepread clotting blocks intact blood vessels

    Severe bleeding occurs because residual blood unable to clot

    Most common in pregnancy, septicemia, or incompatible blood transfusions
  13. Describe Thrombocytopenia
    Bleeding Disorder where there is a deficient number of circulating platelets

    Petechiae (small purplish spots) appear due to spontaneous, widespread hemorrhage

    Due to suppression or destruction of bone marrow (such as cancer, radiation)

    Diagnosed by a platelet count less than 50,000/mm3

    Treatment: transfusion of concentrated platelets
  14. Explain the bleeding disorder of impaired liver function
    Abnormal and sever bleeding occurs

    Inability to sythesize procoagulants

    causes include Vitamin K deficiency, Hepatitis, and Cirrhosis

    Liver disease can also prevent the liver from producing bile, impairing fat, and Vit K absorption (vit K is fat soluable)
  15. What is hemophilia and what are the 3 types?
    Hemophilia: several hereditary bleeding disorders

    • Hemophilia A: most common (77%); due to a deficiency factor in factor VIII
    • Hemophilia B: deficiency of factor IX
    • Hemophilia C: mild tyoe, deficiency of factor IX

    Symptoms: prolonged bleeding, especially into joint cavities

    Treatment: plasma transfusions and injection of missing factors
  16. How do RBCs play a role in human blood grousps?
    • RBC membranes bear 30 types of glycoprotein antigens that are:
    • -perceived as foreign if transfused blood is mismatched
    • -unique to each individual
    • -promotors of agglutination and are called agglutinogens (antigens)

    Presence or absence of each antigen is used to classify blood cells into different groups

    Antigens of the ABO and Rh blood groups case major transfusion reactions

    Other blood groups (MNS, Duffy, Kell, and Lewis) are usually weak agglutinogens
  17. Describe ABO Blood Groups
    A, B, AB, and O

    based on the presence of A and/or B agglutinogens on the surface of RBCs

    blood may contain anti-A or anti-B antibodies (agglutinins) that act against transfused RBcs with ABO antigens not normally present (react)

    Anti-A or Anti-B form in the blood at about 2 months of age

    • O- is the universal Donor because it has no antigens
    • AB+ is the universal receiver because it has no anti-bodies

    • O+ is the most common ABO in US
    • AB- is the lease common ABO in US
  18. Describe Rh blood groups
    There are 45 different Rh agglutinogens (Rh factors)

    C,D,E the most common

    Rh+ indicates the presence of D (85% of USA is Rh+)

    Anti-Rh antibodies are not spontaneously formed in Rh_ individuals

    Anti-Rh antibodies form in an Rh- indicidual receives a Rh+ blood and a second exposure will result in a transfusion reaction
  19. What is Erythroblastosis fetalis?
    Rh- mother becomes sensitized when exposure to Rh+ blood causes her both to synthesize anti-Rh antibodies

    Anti-Rh antibodies can cross the placenta and destroy the RBCS of an Rh+ baby

    Baby can be treated with prebirth transfusion and exchange transfusions after birth

    RhoGAM serum containing anti-Rh can prevent the Rh_ mother from becoming senstized
  20. Describe Tranfusion reactions
    Occurs if mismatched blood is transfused

    • Donor cells...
    • -are attacked by the recipients plasma agglutinins
    • -agglutinate and clog small vessels
    • -rupture and release free hemoglobin into the blood stream

    • Results in...
    • -diminished oxygen carrying capacity
    • -Hb in kidney tubules will cause lethal renal failure
  21. Describe why and how blood volume is restored
    death from shock may result from low blood volume

    • Volume must be replaced immeadiately with:
    • -Normal saline or multiple-electrolyte solution that mimics the plasma electrolyte composition
    • -Plasma expanders that mimic osmotic properties of albumin
    • (but these may be more $$$ and cause significant complications)
  22. Name some diagnostic blood tests
    • Hematocrit
    • Blood glucose tests
    • Microscopic examination reveals changes in RBCs
    • Differential WBC count
    • Prothrombin time and platelet count assess hemostasis
    • SMAC- a blood chemistry profile
    • Complete blood count (CBC)
  23. Discuss the developmental Aspects of Blood
    -Fetal blood cells form in the fetal yolk sac, liver, and spleen

    Red bone marrow is the promary hematopoietic area by the 7th month

    blood cells develop from the mesenchymal cells called blood islands

    The fetus forms HbFm which has a higher affinity for O2 than Hb A formed after birth

    • Blood diseases of the aging:
    • Chronic Leukemias, anemias, clotting disorders-usually precipitated by disorders of the heart, blood vessels, and the immmune system
Card Set
Blood 2 A&P II Lecture
second part of cards for chapter on blood for LCCC's A&P II Lecture