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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 Ca 2+, PF 3, 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*
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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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Explain Coagulation Phase 2: Pathway to Thrombin
- Prothrombin activator catalyzes the transformation of prothrombin to the active enzyme thrombin

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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
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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 clotÂ
- 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
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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
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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
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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
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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
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Name two kinds of disorders the interfere with Hemostasis
Thromboembolytic disorders: undesireable clot formation
Bleeding Disorders: abnormalities that prevent clot formation
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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
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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
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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
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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)
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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
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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
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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
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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
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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
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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
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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)
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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)
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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
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