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pathophys - hematology - WBCs

Where are my study guides for infection, stress and hematology-RBCs located lmfao - they were input into quizlet.com because THIS site was down yesterday
leukocytosis >10,000 WBCs evidencing body protecting itself
leukopenia <5,000 WBCs caused by radiation, chemo, anaphylaxis, SLE
at what WBC count at risk for infection <1,000 at risk
at what WBC count at risk for life threatening infection <500 at risk
normal neutrophil count 2,500-7,500
granulocytosis increase in granulocytes, often used to describe neutrophilia
neutrophilia when neutrophils >7,500
neutropenia when neutrophils < 2,500
shift to left indicates when demand for neutrophils exceeds supply - immature neutrophils being released - such as full-fledged inflamm response
shift to right indicates that inflamm/immune response subsided and neutrophil demand equals supply
neutropenia <2,500 neutrophils, a form of granulocytopenia or agranulocytosis. seen in chemorx
lymphocytosis excess of lymphocytes, usually bwo acute viral inf, some bact inf
lymphocytopenia decreased lymphocytes bwoneoplasias, immune deficiency, drug/radiation/virus destruction
MOA infectious mononucleosis/EBV widespread Bcell invasion---swollen lymphoid tissue due to B-cell antibody production, T-cell prolif.
how does infectious mononucleosis/EBV manifest portal of entry -->sore mouth, throat, fever
leukemia definition malignant disorder of leukocytes, which crowd out normal cells. evidenced by early release of immature WBCs.
common features of leukemias uncontrolled proliferation of leukocytes---overcrowding in bone marrow---decreased production/function of normal hematopoetic cells
MOA acute leukemia NOT caused by rapid proliferation, rather by blocking of blood cell precursors.
what characterizes acute leukemia characterized by neoplastic proliferation of undifferentiated leukocytes called blast cells.
what characterizes chronic leukemia characterized by neoplastic proliferation of more mature leukocytes.
why is leukemia an unusual malignancy there is not an increase in the rate of cell division but rather a blockage of the normal differentiation of the cell so that it continues to divide (“immortal cell”).
what leukemia most common in adults AML acute myelogenous leukemia most common (undifferentiated myelogenous blast)
what leukemia most common in kids ALL acute lymphotic leukemia most common (undifferentiated lyphoblast)
what leukemia arises from Philadelphia xome translocation of 9,22 CML chronic myelogenous leukemia most common (partially differentiated myelogenous precursor)
what leukemia most common in elderly CLL chronic lymphocytic anemia most common (neoplastic proliferation of B-cell precursors)
myeloma malignant tumor formed by cells of bone marrow --> malignant plasma Bcells
MOA of multiple myeloma (B-cell cancer) malignant plasma cells over-produce IgG --> high M PROTEIN, ineffective antibodies -->recurrent infections
Malignant B-cells with Bence Jones proteins (free light chains of Ig) do what they damage renal tubular cells
multiple myeloma - what if neoplastic B-cells accumulate in bone marrow they stimulate osteoclasts --> pathological fractures --> hypercalcemia --> neuro(weakness, confusion, fatigue)
take home message of manifestations of multiple myeloma (B-cell neoplasm) infections, damage renal tubular cells, pathological bone fractures
how are malignant lymphomas classified Hodgkin's lymphomas, non-Hodgin's lymphomas
MOA of Hodgkin's lymphoma abnormal xomes in lymphoid REED-STERNBERG cells
how does Hodgkin's lymphoma manifest usually enlarged painless mass in neck, pain from mechanical pressure/obstruction from other lymphadenopathy
Treatment of Hodgkin's lymphoma chemo/radiation has good survival rate at all phases of disease state UNLESS relapse occurs with 2 years
MOA of non-Hodgkin's lymphoma etiology unknown, greater incidence in immunosuppressed
manifestations of non-Hodgkin's lymphoma painless enlargement of lymph nodes over mo/years. long survival rate
normal range of platelets 140,000 - 340,000 normal
at what platelet count at risk for bleeding from minor trauma <50,000 platelets
at what platelet count at risk for severe or fatal bleeding <10,000 platelets
primary or secondary thrombocytopenia platelets <140,000. can be acute or chonic
MOA primary thrombocytopenia idiopathic = ITP. ----autoantibodies destroy platelets ----HIT = heparin induced thrombocytopenia
MOA secondary thrombocytopenia drug hypersensitivities, bac/vir infections, some autoimmune
thrombocytosis AKA thrombocytopenia platelets > (340,000?) > 400,000
what happens if platelets exceed 1 million likely a thrombosis
MOA of thrombocytosis causes coagulation problems ---clotting factors---Vit K for factors 2,7,9,10----liver disease impairs clotting factor synthesis
what is thromboembolitic disease piece of thrombus embolizes and travels (heart, brain, lung may be lethal)
what is DIC disseminated intravascular coagulation----defective or deficient clotting factors
MOA of DIC cause both hemorrhage AND thrombosis. consumption of platelets, coag factors with widespread fibrin formation in sm/med vessels
Clinical manifestation of DIC severe bleeding, organ damage (ischemia), blood loss
what causes DIC sepsis, severe trauma, liver dx, some treatments like intra-aortic balloon pump
What does Triad of Virchow tell us these are factors that contribute to thrombosis
What are the Triad of Virchow factors loss of vessel wall integrity---abnormal blood flow---alterations in blood constituents
Created by: lorrelaws