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Patho WBCs

Patho Hematology - WBCs

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