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58 Cards in this Set
- Front
- Back
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describe structure of RBC
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biconcave
anucleate large surface:volume for easy gas exchange |
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how do RBCs derive energy
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glucose
90% anaerobic resp 10% HMP shunt |
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survival time of RBC
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120 days
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what does membrane of RBC contain
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chloride-bicarb antiprot
allows RBC to transport CO2 from periphery to lungs for elimination |
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WBC differential from highest to lowest:
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Neutrophils Like Making Things Better
Neutrophils Lymphocytes Monocytes Eosinophils Basophils |
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which WBC are granulocytes
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BEN
basophils eosinophils neutrophils |
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which WBC are mononuclear cells
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monocytes
lymphocytes |
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what are the steps in forming a granulocyte
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pluripotent hematopoietic cell
myeloid stem cell promyelocyte myelocyte metamyelocyte stab cell granulocyte |
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what are the precursors to monocyte
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pluripotent hematopoietic stem cell
myeloid stem cell monoblast monoctye |
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what are the precursors to lymphocytes
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pluripotent hematopoietic cell
lymphoid stem cell lyphoblasts B/T cell |
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what are the steps to RBC formation
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pluripotent hematopoietic stem cell
proerythroblast reticulocyte RBC |
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what are hte steps to platelet formation
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pluripotent hematopoietic stem cell
myeloid stem cell megakaryoblast megakaryocyte platelet |
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what are granulocytes, platelets, and monocytes all derived from (what is common precursor)
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myeloid stem cell
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what is contained in the granules of basophils
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heparin
histamine LTD4 other vasoactive amines |
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when is basophilic stippling seen
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thalassemia
anemia of chronic dz iron deficiency anemia lead poisoning |
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what do eosinophils react to?
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helminths and protazoa
phagocytose ag-ab complexes |
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causes of eosinophilai
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NAACP
neoplastic asthma allergies collagen vascular dz parasites |
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what is contained in the PMNL granules
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hydrolytic enzymes
lysozyme MPO lactoferrin |
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where do B cells go after they are mature?
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migrate to peripheral lymphoid tissue (follices of LN, white pulp of spleen, unencapsulated lymphoid tissue)
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when does B cell --> plasma cell
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when it encounters ag
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appearance of plasma cell
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off center nucleus
abundant RER well developed golgi |
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causes of DIC
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STOP Making New Thrombi
Sepsis (gram -) Trauma OB complications Pancreatitis (acute) Malignancy Neoplasm Transfusion |
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causes of extravascular hemolytic anemia
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odd shapes of RBC (spherocytes, target cells, schistocytes, etc)
autoimmune anemia |
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causes of intravascular hemolytic anemia
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destruction via complement and lysis
paroxysmal nocturnal hemoglobinuria microangiopathic anemia |
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microangiopathic anemia
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seen when theres is an occlusion of a small BV, which leads to mechanical disruption of RBC (seen in DIC, TTP/HUS, SLE, malignancy)
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jaundice in the hemolytic anemias
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not seen in intravascular hemolysis normally, b/c the macrophages eat all of the destroyed Hb
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what is haptoglobin
levels during hemolysis |
a "suicide protein" that carries Hb to the spleen to get broken down
levels are low |
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treatment for spherocytosis
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splenectomy
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process behind paroxysmal nocturnal hemoglobinuria
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acidosis normally develops during sleep, which predisposes cells to destruction via complement, but this is normally inhibited by DAF (which degrades complement); if not enough DAF --> lysis of RBC InTRAVASCULARLY!
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how to dx G6PD deficiency during acute crisis?
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look at blood smear and look for Heinz bodies
when crisis is over, look for enzyme deficiency |
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how to dx autoimmune hemolytic anemia
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direct coomb's test (or indirect)
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some kids can have extremely elevated wbc counts (>50,000) and this is not malignancy... what is it called?
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leukemoid reaction
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why do howell-jolly bodies appear in pts w scd?
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if pts had working spleens, they would have been able to remove these abnormal cells
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what should all SC pts be vaccinated against
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s. pneumonia
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#1 cause of osteomyelitis in SCD
#2 cause? |
salmonella
s. aureus |
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why is hydroxyurea effective in treating SCD?
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it creates an incresae in HbF, which binds to O2 tighter than adult Hb.
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what would you do with an african american person who presents with microscopic hematuria, and is asymptomatic and has a normal CBC?
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test for SCD!!
there may be sickling in the renal medulla and peritubular capillary (so they might be a carrier of the trait) |
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what does antithrombin III do?
what activates it? |
breaks down factors IX, X, XI
heparin |
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factor V leiden?
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factor 5 is resistant to breakdown by APC
leads to venous clots |
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protein c
what does it require |
breaks down factors V and VIII
requires vit K and protein s |
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protein s
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required as a cofactor for APC
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tPA
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activates plasmin, which breaks down fibrin
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difference between multiple myeloma and waldenstrom's macroglobulinemia
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MM: IgG or IgA in high amounts (lytic bone lesions, renal insuff from increased Ig light chains excretion - Bence Jones proteins)
W<: IgM in large amts (--> hyperviscosicty, no lytic bone lesions) both have M spike |
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which form of hodgkin's lymphoma has the worst prognosis
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lymphocyte depleted
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translocation (9;22)
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Philadelphia chromosome
CML |
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translocation (8;14)
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Burkitt's lymphoma (c-myc activation)
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translocation (14;18)
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follicular lymphoma (bcl2 expression)
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translocation (15;17)
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M3 - AML
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translocation (11;22)
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ewing sarcoma
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translocation (11;14)
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mantle cell lymphoma
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when is WAIHA seen
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chronic anemia seen with:
SLE CLL some drugs |
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when is CAIHA seen
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infectious mononucleosis
m. pneumonia |
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which NHLs are seen in children
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burkitt's lymphoma
diffuse large cell lymphoblastic lymphoma |
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smudge cells
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cll
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philadelphia chromosome
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cml
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auer rods
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aml
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how to differentiate cml from leukemoid reaction
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cml has low alk-phos levels
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what is a result of treating aml
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cells can release auer rods --> DIC
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