Chapter 10 Alterations in Hemostasis

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Chapter 10
Alterations in Hemostasis
Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins
Hemostasis
• Stopping blood flow
• Normal:
– Blood usually fluid
– Seals broken blood vessels
• Abnormal:
– Inappropriate clotting
– Insufficient clotting
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Platelets (Thrombocytes)
• Thrombopoietin
– Made in liver, kidney, smooth muscle,
bone marrow
• Megakaryocytes formed in bone marrow
– Break apart to form many platelets
• Platelets live 8–9 days in circulation
– Many are stored in spleen
– Released when needed
Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins
Question
All but which of the following are true about platelets?
a. An enzyme called erythropoietin stimulates their
production.
b. They are made from megakaryocytes.
c. They originate from the bone marrow.
d. They are stored in the spleen.
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Answer
a. An enzyme called erythropoietin stimulates their
production.
Rationale: Erythropoietin stimulates the production of
RBCs (erythrocytes). The word literally means
erythrocyte production. Platelet formation is stimulated
by thrombopoietin (thrombus/clot production).
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Mediators of Hemostasis
• Chemicals produced by platelets
• Released at an injury to:
– Start clotting by reacting with blood proteins
– Help platelets stick together
– Stimulate wound healing
– Help platelets stick to vessel wall
– Constrict blood vessels
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Coagulation Factors
• Plasma proteins
– Most are synthesized by liver
– von Willebrand factor made by
endothelium
– Circulate as inactive procoagulation factors
• Calcium
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Question
What is the effect of von Willebrand disease on the
platelets?
a. Increased platelet aggregation
b. Decreased platelet aggregation
c. Increased platelet formation
d. Decreased platelet formation
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Answer
b. Decreased platelet aggregation
Rationale: Von Willebrand disease is the most common
hereditary bleeding disorder. It is caused by a deficiency
or defect in vWF (which carries a clotting factor). The
result of less clotting factor is an inability to clot.
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Vessel Spasm
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Cyclooxygenase Enzymes (COX)
Produce Mediators of Hemostasis
• Celebrex is a drug
that blocks COX-2
• People taking
Celebrex develop
increased TXA2
levels
• What problems
might they have?
arachidonic
acid
COX-1 COX-2
thromboxane A 2
prostacyclin
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Intrinsic and Extrinsic Pathways
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Fibrinogen  Fibrin
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Scenario
A man had a stroke and the doctor gave him tissue
plasminogen activator (TPA).
• Why? What is the doctor trying to accomplish?
• One of the man’s relatives wondered why they did
not give him heparin or warfarin instead
– What is the difference? Why might TPA be
more appropriate?
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Hypercoagulability
• Increased platelet number
• Platelet aggregation
• Endothelial damage
• Increased procoagulation factors
• Decreased anticoagulation factors
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Question
Tell whether the following statement is true or false.
Hypercoagulability states increase the risk of thrombus
formation.
Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins
Answer
True
Rationale: Hyper- as a prefix means “over” or “too much.”
Coagulation/coagulability means “clotting/the ability to
clot.” Hypercoagulability means “increased ability to clot
or form thrombi.”
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Scenario:
A woman with lupus develops breast cancer.
• She is given radiation therapy
– She begins to develop nosebleeds and bruising
– Her menstrual period is abnormally heavy
Question:
Why did this happen?
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Platelet Disorders
• Decreased platelet levels (thrombocytopenia)
– Decreased production
– Increased destruction
– Platelets used up in forming clots
• Impaired platelet function
Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins
Question
Tell whether the following statement is true or false.
Platelet disorders are bleeding disorders.
Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins
Answer
True
Rationale: Because the platelet’s job is to clot, platelet
disorders mean that the platelets cannot do that job. An
inability to clot results in bleeding/bleeding disorders.
Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins
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