B. Platelets 1. Myeloid tissue megakaryocytes thrombocytes (platelets)

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1 I. Hemostasis A. Define hemostasis vs. hemorrhage 1. Hemostasis 2. Hemorrhage B. Platelets 1. Myeloid tissue megakaryocytes thrombocytes (platelets) 2. Platelets are packed with chemicals a. Alpha granules Clotting factors Platelet derived growth factor (PDGF) b. Dense granules (clotting factors and other products important for platelet plug formation see below) B. 3 major processes of hemostasis (Describe each) 1. Vessel spasm in response to vessel damage a. Direct stimulus and blood vessel spasm Pain receptors in tissues Mainly in smaller vessels b. Granules release serotonin vasoconstriction 2. Platelet plug formation (Fig. 19.9, pg. 681) a. Vessel damage roughened endothelial surface b. Platelet adhesion c. Aggregation and agglutination d. Platelet release reaction discharge of granules 1) ADP and thromboxane A2 (=prostaglandin) 2) Serotonin and epinephrine and thromboxane A2 e. Positive feedback mechanism f. Platelet plug is effective for? g. Larger vessels? h. More serious injuries clotting and/or medical intervention Revised Spring

2 3. Coagulation (blood clotting) Definition of coagulation Homeostatic mechanism a. Serum vs. plasma (previous notes) Serum Plasma b. Clot vs. anticoagulant c. Clotting vs. agglutination d. Thrombosis vs. hemorrhage e Clotting factors 1) 12 chemical factors involved (See Table 19.4) 2) Roman numerals 3) Produced in liver, cells (tissue cells, endothelial cells lining blood vessels), platelets, or from diet 4) Found in plasma or in platelets or in tissues 5) Reactions involve a cascade of reactions and may take one of two pathways initiated by either: tissue damage (tissues release tissue factors) platelets broken over roughened vessel endothelium (platelets release platelet factors) or both simultaneously 6) In either case fibrinogen (soluble form) is converted to fibrin threads (insoluble form) and the result is a CLOT. (See Fig , pg. 682) II. Blood Clotting Cascade (Fig , pg. 683) A. Stage 1 1. Extrinsic pathway 2. Intrinsic pathway 3. Factor X 4. Prothrombin activator (prothrombinase) Revised Spring

3 B. Stage 2 1. Common pathway 2. Prothrombin Thrombin C. Stage 3 1. Fibrinogen fibrin threads 2. White clot 3. Red clot 4. Factor XIII (fibrin stabilizing factor) 5. Positive feedback loops initiated by thrombin a. Stimulates formation of prothrombinase (prothrombin activator) more thrombin b. Activates platelets more platelet aggregation and agglutination D. Syneresis clot retraction 1. Due to platelet activity 2. Processes of platelets 3. Contraction 4. Serum E. Fibrinolysis dissolution of clot 1. Plasminogen plasmin 2. Dissolves clot Revised Spring

4 Trauma initiates both pathways: extrinsic (tissue factors) and intrinsic (rough surface of broken vessels causes release of platelet factors). How does this compare with blood clotting in a glass, non-heparinized test-tube? III. Prevention of coagulation A. Smooth endothelium B. Fibrin absorbs thrombin into the clot and isolates it C. Dispersal of clotting factors reduces concentration and interaction of clotting factors. D. Inhibitors of platelets E. Anticoagulants (see anticoagulants aspirin and thrombolytic agents, page 685) 1. Antithrombin agents (inhibit thrombin) 2. Other factor inhibitors 3. Heparin (basophils and mast cells basophils become mast cells in tissues, common in connective tissue around capillaries) a. Anticoagulant b. Numerous in liver and lungs why? c. Pharmacological anticoagulant (from bovine lung tissue and bovine and porcine intestinal mucosa) d. Fast acting injection almost immediately increases clotting time e. Prevents formation of thrombin f. Hemodialysis and open heart surgery g. The hospital anticoagulant h. Heparinized capillary tube in lab why? 4. Dicoumarol (Coumadin, Warfarin) a. Anticoagulant b. Competes with Vitamin K and interferes with liver synthesis of prothrombin and other clotting factors. c. What is the significance of Vitamin K? d. Takes longer to work hours, but longer lasting e. The take home anticoagulant Revised Spring

5 5. Aspirin a. Prevents? b. Why important to take an aspirin immediately if suspect an MI? Note this is only when other, more serious risk factors of taking aspirin are not present. c. Should you be taking aspirin before surgery? Why/why not? d. Excessive bruising? Exemplifies the fine balance between clotting agents and anticoagulants. 6. Thrombolytic agents a. What are they? b. What do they do? c. Streptokinase d. Tissue plasminogen activator (t-pa) 7. CPD (citrate phosphate dextrose), sodium citrate, and ammonium oxalate) a. What are these products used for? b. Bind calcium so it is not available for clotting c. Why calcium? d. Can be reversed so the blood can regain its clotting ability e Often used in blood banks and for laboratory testing of clotting time f. Not used as human anticoagulant explain. F. Review and outline intravascular clotting (page 685) in detail on own. Revised Spring

6 IV. Coagulation disorders excessive bleeding vs. abnormal clotting A. Liver disease 1. Synthesis of many clotting factors (See Table 19.4) 2. Liver disease associated with bleeding disorders 3. Bile salts needed for absorption of Vitamin K (why is Vitamin K so important?) 4. Gall bladder, blocked bile ducts 5. Why do you give Vitamin K to alcoholics? 6. Vitamin K prophylactically prior to surgery? B. Newborns 1. Low blood levels of certain coagulation factors (liver not up to speed yet?) 2. Prophylactic Vitamin K C. Thrombocytopenia (<100,000 platelets/mm 3 ) D. Leukemia and other cancers (crowd out platelets or platelet forming cells in red bone marrow) see also p. 690 E. Disseminated Intravascular Clotting (DIC) F. Hemophilia (see also pp ) 1. Hereditary mainly in 2. Deficient in various blood clotting factors 3. Classic hemophilia Hemophilia A missing factor? 4. Hemophilia B missing factor? (also called Christmas Factor) 5. Symptoms of either type of hemophilia are all similar Revised Spring

7 a. Frequent nosebleeds b. Large intramuscular hematoma c. Hematuria (blood in urine) d. Severe pain and disability from bleeding into joints and body cavities. e. May be due to trauma or may be spontaneous 6. Treatment a. Pressure packing/control bleeding b. Transfusions c. Additional risk 1) Hepatitis 2) HIV/AIDS 3) A generation of hemophiliacs with AIDS 4) Things look a lot better now blood testing, plasma, concentrated clotting factors 5). Why does a hemophiliac have some ability to stop bleeding? Think!!! Revised Spring

Thibodeau: Anatomy and Physiology, 5/e. Chapter 17: Blood

Thibodeau: Anatomy and Physiology, 5/e Chapter 17: Blood This chapter begins a new unit. In this unit, the first four chapters deal with transportation one of the body's vital functions. It is important