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NURS 350 WBC
pathophys - hematology - WBCs
| Question | Answer |
|---|---|
| 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
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