Patho Ch 12

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Patho Ch 12
2014-10-29 19:35:13
Exam #4
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  1. Platelets (Thrombocytes)

    Normal range:
    150,000 - 400,000

    Critical: <50,000 or >999,000

    increased⇢thrombocytosis: spleen problem (low/no function); cancer

    decreased⇢thrombocytopenia: bone marrow suppression, cancer, sepsis, liver failure, malnutrition

    live 8-9 days in circulation

    stored in spleen and released when needed
  2. Thrombopoietin


    • Made in liver, kidney, smooth muscle, bone marrow
    • ___________________________________

    Formed in the bone marrowbreak apart to form many platelets
  3. Mediators of Hemostasis (the stopping of the flow of blood)
    =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
  4. Coagulation Factors
    Plasma proteins:

    • -most are synthesized by the liver
    • -von Willebrand factor made by endothelium
    • -circulate as inactive procoagulation factors
    • -each factor is identified by Roman numeral; performs a specific step in the coagulation process or "cascade"

    Calcium: for factor IV and all but first two steps

    Vitamin K: necessary for production of VII, IX, X, prothrombin, and protein C

    A clot is not a permanent solution to vessel injury

    Thrombin: an enzyme in blood plasma that causes the clotting of blood by converting fibrinogen to fibrin.
  5. Intrinsic and Extrinsic Pathways
  6. Hypercoagulability
    • increased platelet number
    • platelet aggregation
    • endothelial damage
    • increased procoagulation factors
    • decreased anticoagulation factors
    • may be inherited (Leiden mutation); prolonged bed rest; sickle cell disease; oral contraceptives; smoking; obesity; antiphospholipid sydrome
  7. Platelet disorders
    Decreased platelet levels (thrombocytopenia)

    • -decreased production
    • -increased destruction
    • -platelets used up in forming clots

    Impaired platelet function

    Immune thrombocytopenic purpura (immune system destroys platelets which are necessary for normal blood clotting); drug-induced thrombocytopenia


    • ITP- occur because of viral infection (mumps or the flu), during pregnancy, or immune disorder (lupus or HIV): 80% cases in kids go away after 6 months w/o treatment, but adults will most likely need treatment
    • Women more susceptible than men
    • See most often in elderly
  8. Von Willebrand Disease
    • Most common hereditary bleeding D/O
    • Deficiency/defect in vWF; in men and women
    • Usually autosomal dominant disorder
    • Many variants; defect in platelets and coagulation pathway; causes: decreased platelet aggregation and decrease clotting
    • Spontaneous bleeding from nose, mouth, GI; heavy menses; prolonged bleeding time
    • Bleeding usually mild; avoid aspirin; treat with Desmopressin
  9. Hemophilia A
    • X-linked recessive D/O; primarily affects males
    • may also be from new mutation
    • insufficient or deficient Factor VIII
    • Mild, moderate, severe forms
    • bleeding in soft tissues, GI, hip/knee/elbow/ankle; chronic bleeding in joints causes fibrosis (thickening and scarring of connective tissue) and contracture (shortening and hardening of muscles, tendons, and other tissue)
    • intracranial hemorrhagemajor cause of death
    • prevent trauma; avoid aspirin/NSAIDS (nonsteroidal anti-inflammatory drugs); Factor VIII replacement; in past, high contamination with HIV due to tainted blood
  10. Other Disorders of Platelets
    • Acquired disorders
    • Liver disease
    • Vitamin K deficiency
    • Vascular disorders
    • Vitamin C deficiency: scurvy
    • Senile purpura (bruising): bruising in elderly from impaired collagen
  11. Disseminted Intravascular Coagulation
    • Paradox of widespread coagulation and bleeding
    • Complication of many disorders
    • Begins with massive activation of coagulation sequence; leads to fibrin deposition; form thrombi; leads to tissue ischemia (inadequate blood supply to an organ or part of the body); hemolytic anemia from fragmented RBCs; platelets and coagulation factors get used up; activation of plasminogen; leads to hemorrage (bleeding)