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22 Cards in this Set
- Front
- Back
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Peripheral Leukocyte Response to Infection or Injury |
•Response to bacterial Infection: Granulocytosis (mainly neutrophils)
•Response to viral Infections: Lymphocytosis
•Response to parasitic Infections: eosinophils, eosinophilic leukocytes |
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Peripheral Leukocyte Response to Infection or Injury |
•Band neutrophils (immature cell) and left shift occur following severe injury and bacterial sepsis
•Infectious mononucleosis: (Lymphocytosis) Self-resolving, young people. Caused by Epstein-Barr Virus infecting B-lymphocytes |
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Lymph Node Response to Injury or Infection |
•Lymphadenopathy: enlarged, swollen nodes •Lymphadenitis: Infection of a lymph node -Reactive hyperplasia / reactive lymphadenitis: lymph node is not itself infected, just responding |
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Lymph Node Response to Injury or Infection |
•Cat scratch disease (subacute regional lymphadenitis) - a Rickettsia-like microorganisms Infection, children, teens |
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Lymphoid Neoplasms |
•Acute Lymphocytic Leukemia -50% Cure rate •Chronic Lymphocytic Leukemia -B-cell. Prone to Infection, 10-year survival typical |
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Lymphoid Neoplasms |
•Lymphoma -Hodgkin Lymphoma: Starts with Epstein-Barr Virus in immuno-compromised pts. Defense T-Cells |
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Lymphoid Neoplasms |
Lymphoma •Non-Hodgkin lymphoma: B cells aggressive -Diffuse type: Abnormal histology; aggressive -Follicular type: Microscopic pattern resembles normal lymphoid follicles; less aggressive; better prognosis |
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Myeloid Neoplasms |
Myeloid Leukemia •Acute myeloid leukemia: Immature WBCs present -Primary disease, or -Evolution from chronic Myeloproliferative disorder. Young 50% 5 yr survival rate Older patients 10% 5 yr survival rate |
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Myeloid Neoplasms |
•Chronic myeloid leukemia: Mature WBCs (>100,000!!) -Primary disease, or -Evolution into other myeloproliferative disorders or -Evolution into acute myeloid leukemia |
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Disorders of the Spleen and Thymus |
Spleen: •Splenomegaly: Enlarged spleen
•Hypersplenism: Overactivity of Spleen -Consumes more than the normal amount of WBC, RBC, or platelets -Hypersplenism is associated with enlarged spleen |
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Disorders of the Spleen and Thymus |
Thymus: •Hereditary immune deficiency (T-cell deficiency)
•Mysathenia gravis -Hyperplasia or Thymoma in 50% of Cases |
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Normal Hemostasis, Coagulation, and Lab Testing |
A. Injury Occurs B. Temp. Vasoconstriction occurs C. Blood contacts tissue, platelets accumulate, Coagulation D. Further platelet aggregation occurs, and coagulation produces a web of fibrin in the wound E. Hemorrhage stops as fibrin traps red cells, blocks bleeding |
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Hemostasis |
•Hemostasis and its tests -Prothrombin Time -Partial Thromboplastin Time
•Vascular factors, Coagulation, and platelets play roles |
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Hemostasis Tests |
Prothrombin Time: •Tissue Trauma •Tissue Factors |
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Hemostasis Tests |
Partial Thromboplastin Time: •Blood contact with foreign surface |
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Bleeding Disorders Major Determinants of Disease 1 |
•Excess bleeding is always associated with at least one of three factors: 1. Fragile blood vessels 2. Low platelet count or defective platelet function 3. Decreased coagulation factor activity |
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Bleeding Disorders Major Determinants of Disease 2 |
•Bleeding related to platelet disorders usually occurs from capillary-sized blood vessels •Bleeding related to coagulation factors usually occurs from larger vessels |
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Bleeding Disorders Major Determinants of Disease 2 |
•Most coagulation factors are proteins made by the liver, and severe liver disease is often accompanied by excessive bleeding.
•Intravascular clotting is always abnormal and secondary to another disease. |
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Bleeding Disorders: Vascular or Platelet Deficiency |
•Bleeding from fragile blood vessels (Vasculitis, Vit-C deficiency) •Bleeding for low platelet count or platelet malfunction (capillary sized vessels, petechiae, nosebleed, hematuria, menses) -Toxins, drugs -Marrow Failure -Hypersplenism -Immune thrombocytopenia Purpura (ITP) -Need Spleenectomy? |
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Coagulation Factor Deficiency |
Causes: •Vit-K Deficiency •Liver disease (most made here) •Genetic defects -Hemophilia A (X-linked, Factors VII) -Hemophilia B (X-linked, Christmas factors IX) -Von Wielbrand Disease (VW Factor) |
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Coagulation Factor Deficiency |
Causes: •Intravascular coagulation (Disseminated Intravascular coagulation (DIC)) |
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Thrombotic Disorders |
•Lupus anticoagulant: Auto-immune antibody, interferes with tests, looks like poor coagulation but opposite is true (venous thrombosis) •Factor V Leiden: Genetic defect deactivating Coagulation Factors V = venous thrombosis •Again note: Blood normally clots outside vessels, not inside (pathological). |
