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Patho WBCs
Patho Hematology - WBCs
| Question | Answer |
|---|---|
| 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
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