Patho Hematology - WBCs
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| normal leukocyte range | 5,000 - 10,000 cells/mcL
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| disease state when white cells >10,000 | leukocytosis
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| disease state when white cells < 5,000 | leukopenia
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| Lab value of leukocytes when risk of infection, risk of lethal infections | <5,000 and <1,000
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| what is the most abundant granulocyte | neutrophils
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| normal range of neutrophils | 2,500 - 7,500
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| Under what conditions do neutrophil counts increase - 3 | infections, polycythemia vera, chronic myelocytic leukemia
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| Under what conditions are neturophil counts decreased | infectious process uses them up, or draws them out ciruculation faster than bone marrow can make them, as in chemorx
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| granulocytosis is another word to describe | neutrophilia - condition with neutrophils > 7,500
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| What do we watch for in labs to indicate status of infections | shift to left indicates immature neutrophils being releases as supply exceeds demand (rampant infection) and then a shift to right as infection subsides
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| granulocytopenia or agranulocytosis are other words to describe | neutropenia - labs <2,5000 as in chemorx
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| common causes of leukocytosis | malignancies, hematological dx, pathogens, anesthesia, surgery, pregnancy, drugs/toxins/hormones, strenuous exercise, emotional or temperature changes
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| common causes of leukopenia | radiation, chemorx, anaphylactic shock, SLE
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| infectious mononucleosis virus name and target | Epstein Barr virus targets B-cells
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| lymphocytosis definition and cause | excessive lymphocytes, most common in viral infections, rarely by bacterial infections
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| lymphocytopenia definition and cause | decreased lymphocytes, neoplasias, immune deficiencies, destruction by radiation, drugs, or viruses
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| Name 2 disorders of lymphocytes | infectious mononucleosis (EBV) and leukemias
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| MOA of EBV | virus attaches EBV B-cell receptors, widespread B-cell invasion. Unaffected B-cells make Abs while Tcells attack directly
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| EBV clinical manifestation | lymphoid tissue swollen, sore throat, fever, inflammation in portal of entry - mouth and throat
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| General MOA of leukemias | cancer of bone marrow or blood characterized by abnormal increase in immature WBCs
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| In leukemia a single cell is transformed then prolifereates. Do these leukemic cells divide faster or slower? | leukemic cells dived more slowly and take longer to make DNA (which is why they are immature when released)
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| 3 common features of leukemia | uncontrolled leukocyte growth, overcrowding in bone marrow, decreased production/function of normal hematopoietic cells
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| Name 4 classes of leukemias | ALL acute lymphotic leukemia, AML actue myelogenous leukemia, CLL chronic lymphotic leukemia, CML chronic myelogenous leukemia
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| what, in general causes the symptoms of acute leukemia | NOT caused by rapid proliferation, rather by the accumulation of leukemia cells that then compete with normal cell proliferation.
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| what is leukemia generally characterized by | an increase undifferentiated or imature blast cells
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| what are general s/s of anemia in general | bone marrow depression, chronic fatigue (anemia), bleeding (thrombocytopenia), infections causing fever, anorexia, enlargement of liver, spleen and lymph nodes
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| What charcterizes ALL (transformed blast)and who most commonly gets it | >30% increase in lymphoblasts in blood/marrow,children
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| what impact does leukemia malignancy have on cells | accumulations of dysfunctional cells, loss of cell division/regulation
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| AML MOA and who most commonly gets in | acute myelogenous leukemia is abnormal proliferation of myeloid precursors with decreased apoptosis/differentiation. adults
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| what are most common leukemias for child and adult, respectively | ALL and AML
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| In chronic leukemias, what is unique about the cells | predominant cell APPEARS normal but doesn't function properly
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| MOA of EBV | virus attaches EBV B-cell receptors, widespread B-cell invasion. Unaffected B-cells make Abs while Tcells attack directly
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| MOA of chronic leukemias | onset gradual, prolonged clinical course. Remission greatly increased
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| symptoms of Chronic leukemias | splenomegaly, extreme fatigue, weight loss, night sweats, low grade fever
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| EBV clinical manifestation | lymphoid tissue swollen, sore throat, fever, inflammation in portal of entry - mouth and throat
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| General MOA of leukemias | cancer of bone marrow or blood characterized by abnormal increase in immature WBCs
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| In leukemia a single cell is transformed then prolifereates. Do these leukemic cells divide faster or slower? | leukemic cells dived more slowly and take longer to make DNA (which is why they are immature when released)
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| 3 common features of leukemia | uncontrolled leukocyte growth, overcrowding in bone marrow, decreased production/function of normal hematopoietic cells
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| Name 4 classes of leukemias | ALL acute lymphotic leukemia, AML actue myelogenous leukemia, CLL chronic lymphotic leukemia, CML chronic myelogenous leukemia
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| what, in general causes the symptoms of acute leukemia | NOT caused by rapid proliferation, rather by the accumulation of leukemia cells that then compete with normal cell proliferation.
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| what is leukemia generally characterized by | an increase undifferentiated or imature blast cells
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| what are general s/s of anemia in general | bone marrow depression, chronic fatigue (anemia), bleeding (thrombocytopenia), infections causing fever, anorexia, enlargement of liver, spleen and lymph nodes
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| What charcterizes ALL (transformed blast)and who most commonly gets it | >30% increase in lymphoblasts in blood/marrow,children
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| what impact does leukemia malignancy have on cells | accumulations of dysfunctional cells, loss of cell division/regulation
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| AML MOA and who most commonly gets in | acute myelogenous leukemia is abnormal proliferation of myeloid precursors with decreased apoptosis/differentiation. adults
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| what are most common leukemias for child and adult, respectively | ALL and AML
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| In chronic leukemias, what is unique about the cells | predominant cell APPEARS normal but doesn't function properly
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| MOA of chronic leukemias | onset gradual, prolonged clinical course. Remission greatly increased
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| symptoms of Chronic leukemias | splenomegaly, extreme fatigue, weight loss, night sweats, low grade fever
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| take home MOA of lymphocytic leukemias ALL, CLL | cancerous cell transformation in bone marrow effects lymphocytes --> B-cells
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| take home MOA of myelogenic leukemias AML, CML | cancerous cell transformation in bone marrow effects cell lines of RBC, some WBC and platelets
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| the Philadelphia chromosome is involved in what type of leukemia | found in patients with CML
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| how does philadelphia chromosome work? | receptrocal translocation between long arms of 9 and 22. When this happens it becomes the Philadelphia chromosom and triggers excessive production of WBCs. Is present in 95% of those with CML, in other leukemias at lower rates
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| implications of Philadelphia chromosome | historical for genetics, cancer. implication s for children with leukemia and implications for disease treatment
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| What is a myeloma | malignant tumor formed by bone marrow cells
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| what is multiple myeloma | B-cell cancer associated with mature plasma cell structure/function
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| what genetic incident causes multiple myeloma | translocation, usually an aneuploidy with 44 to near tetraploid (4 sets of chromosomes)
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| what is MOA of multiple myeloma | malignant plasma (B) cells --> large amount IgG--> M protein, an abnormal immunogloulin which becomes very prominant in blood --> ineffective Ab production -->clinical disease/infections
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| what protiens are unique to multiple myeloma | M protein and Bence Jones proteins
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| what do Bence Jones proteins do | free light chains of immunoglobulin appear in urine and damage renal tubular cells
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| where do neoplastic B-cells accumulate in multiple myeloma | in bone marrow, where they stimulate clasts -->pathological bone fratures bwo destroying bone cortex
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| what chemistry alteration can occur with respect to multiple myeloma | can result in hypercalcemia -->neurological depression of weakness, confusion,fatigue
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| take home diseases states resulting from multiple myelomas | infections, pathological fractures, hypercalcemia
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| what are 2 broad classes of lymphoid alterations | lymphadenopathy (local, general) and malignant lymphomas (Hodgins, non-Hodgkins)
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| MOA of localized lymphadenopathy | drainage of inflammed lesion
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| causes of generalized lympadenopathy | neoplasms, immune/inflamm, endocrine or lipid storage disorders
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| what are malignant lymphomas generally associated with | tumors of primary or secondary lymphoid tissue
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| what abnormal cell type in Hodgin's lymphoma and what it does | familial clustering of unknown genetic mechanism and/or viruse --> abnormal lymph node chromosomes appearing as REED-STERNBERG cells
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| s/s Hodgkin's lymphoma | enlarged, painless neck mass due to pressure and obstruction from resultant lymphadenopathy
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| tx of Hodgkin's lymphoma | chemo/radiation possible at all disease states. relapse in 2 years has poor prognosis
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| what is etiology of non-Hodgkin's lymphoma | unknown etiology but great incidence in those who are immunosuppresed
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| s/s of non-Hodgkins | painless enlargement of lymph nodes over months/years. usually long survival rate
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| what is the normal range for platelets | 140,000 - 340,000
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| what is thrombocytopenia | not enough platelets <100,000
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| what is risk at platelets < 50,000 | risk of bleeding from minor trauma
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| what is risk at platelets 10,000 - 20,000 | petechia-purpura-ecchymosis (bleeding under skin, graded by size in cm up to 1 cm)
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| what are the 2 types of thrombocytopenia | primary (acute, chronic) and secondary
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| another name for primary thrombocytopenia | ITP = idiopathic thrombocytopenia purpura
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| MOA of ITP/primary thrombocytopenia | either by autoantibody destruction of platelets or HIT heparin inducted thrombocytopenia
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| what causes secondary thrombocytopenia | drug hypersensitivities that produce (auto)antibodies, bacterial/viral infections, some autoimmune diseases
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| what is thrombocytosis | too many platelets >400,000
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| clinical significance of platelets >1 million | results in thrombosis
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| what are some causes of coagulation problems | diseases in: clotting factors, Vit K (2,7,9,10), liver (impairs clotting factor synthesis)
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| what is a thromboembolic disease | where all/part of thrombus breaks away and travels as embollus. can lodge in heart, lung, brain and be fatal
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| what is the Triad of Virchow | loss of vessel wall integrity, abnormal blood flow, alterations in blood constituents
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| what is another method by which clots can form | insufficient anti-coagulation factors or conditions that promote venous stasis
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| one form of consumptive thrombo-hemorrhagic disorder | DIC = disseminated intravascular coagulation
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| what is DIC disseminated intravascular coagulation | its an acquired syndrome with widespread fibrin formation in small-medium blood vessels
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| what is MOA of DIC | accumulation of fibrin in small-medium bessels leads to consumption/trapping of platelets and coagulation factors. They can't do their job and severe bleeding, organ damage and blood loss can occur
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| what causes DIC | caused by sepsis,severe trauma, liver disease, intra-aortic balloon pump and like treatments
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