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409 Cards in this Set
- Front
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true positive rate
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Sensitivity
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ability of the test to identify positive results in pts who have disease
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Sensitivity
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lower chance of false negative result
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higher sensitivity
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higher cange of false negative result
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lower sensitivity
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% of negative results in people without disease
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Specificity
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true negative rate
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specificity
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the higher the chance of a false positive result
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specificity
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PSA-specific for prostate but not prostate carcinoma
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specificity
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ESR- erythrocyte sedimentation rate
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specificity
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contains nothing or something to activate formation of clot
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red top tube
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anticoagulant, EDTA, prevents blood from clotting, cells separate
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purple top tube
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preserves the cells so they can e identified by how they look with stains
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purple top tube
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anticoagulant, sodium citrate, preserves more clotting factors
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blue tube
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tube is used to evaluate the ability of the blood to clot
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blue tube
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plain, blood clots, provides serum for testing
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red top tube
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fel forms barrier between serum and cells during centrifugation
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tiger top tube
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serum separator tube
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tiger top tube
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sodium fluoride oxalate, prevents glycolysis, glucose tolerance testing
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gray top tube
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EDTA prevents clottign, used in hematology for CBCs
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purple top tube
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sodium citrate, used for coagulation (Pt/INR, prothrombin times, (PTT)
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blue top tube
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used for blood culture collection, may use aerobic and anaerobic bottles
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Yellow top
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heparin, prev clotting, provides plasma-ammonia &carboxyhemoglobin test
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Green top tube
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liquid portion of the blood
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plasma
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the clot forming components
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platelets
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the infection fighers
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WBC
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the oxygen transporters
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RBC
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serum or plasma portion of blood after centrifugation (depends on if anticoagulant was used)
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top layer
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consists of WBCs and platelets after centrifugation
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buffy coat - middle layer
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consists of rbc after centrifugation
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bottom layer
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blood collected without an anticoagulant produces
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serum
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blood collected with an anticoagulant produces
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plasma
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contains fibrinogen and clotting factors
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plasma
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does NOT contain clotting factors, they are used up with clotting factors to form clot
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serum
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amt of blood made up of RBCs (erythrocytes), WBC(leukocytes), and platelets
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45%
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amt of blood made up of plasma of which 90% is H2O 10% proteins salts, CHO, enymes lipids
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55%
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oxygen from lungs to tissue
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transport funct of blood
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water and nutrients
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transport funct of blood
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cellular elements that fight infection and aid coagulation
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transport funct of blood
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waste products for excretion through skin, kidneys, lungs
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transport funct of blood
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the process of blood development and production
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hematopoiesis
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produced from a multi-potential stem cell in the bone marrow
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all cells
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colony stim factors and inerleukins infl stem cell to div and diff into two major cell lines - irreversible
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myeloid or lymphoid
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leukocytes are divided into 2 groups
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granulocytes & agranulocytes
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include neutrophils(segs, polys, PMNs), eosinophils and basophils
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granulocytes
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possess multi-lobulated nuclei and derive their name from the granules found in their cytoplasm
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granulocytes
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a granular, mononuclear cells
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lymphocytes
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production of neutrophils, eosinophils, basophils, and monocytes
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myelopoiesis
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process of development from immature blast to mature cell takes approx
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7-10dys
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at the end of DNA synthesis they (blood cells) are in a
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maturation pool
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once matured they(blood cells) become part of a functional
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functional pool
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percentage of blood circulating and percentage of blood adhere to lining of vessel walls
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50%
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adequate ratio of blood sample to anticoagulant is required for
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sample collection
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tot WBC reported as
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#wbc/mm3
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highest at birth then slow fall to adult levels, lymphocytes predominate from 2wks to age 5-7, then PMN predomin
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WBC
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highest at birth, lowest at 3 mnths, higher in males, nl decreases in pregnancy
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hemoglobin (g/dl)
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conjugated protein consisting of globin, protoporphyrin, and iron
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hemoglobin (g/dl)
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depends on adequate Fe supply & delivery, synthesis of protoporphyrins, and globin synthesis
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hemoglobin (g/dl)
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<8 and >20g/dl
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panic values of hemoglobin
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package cell volume =usually 3 X hemoglobin, reported as a %
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hematocrit
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<24%
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panic value of hematocrit
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inc'd in polycythemia vera, smokers, high altitude(hypoxia stim RBC prod), dehydration (dec fluid & vol, same #rbc
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hematocrit
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dec'd in megaloblastic anemia(folate or B12 def), blood loss, drug/alcool addic, Fe def, sickle cell anem, pregnancy
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hematocrit
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40-54%
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hematocrit male value
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37-47%
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hematocrit female value
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50-62%
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hematocrit hewborn values
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14-18 g/dl
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nl male value hemoglobin
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12-16 g/dl
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nl females hemoglobin values
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17-23 g/dl
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nl newborns hemoglobin value
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12-14.5 g/dl
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nl kid hemoglobin values
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mean cell volume, avg volume of rbc, kids have lower values than adults, for every yr under 10 subtract 1 from 80
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MCV
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Hct/RBC
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MCV
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mean cell hemolgobin - the weight of hemoglobin of averg RBC
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MCH
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Hgb/RBC
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MCH
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mean cell hemoglobin conc- the avg concentration of hemoglobin in a given vol of red cells
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MCHC
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Hgb/Hct
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MCHC
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red cell distribution width a measure of the degree of anisocytosis, measured by automated counters
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RDW
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variation in RBC size
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anisocytosis
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nl 11.5-14.5%
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RDW
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helpful with distinguishing unclomplicated thalessemia from early iron def anemia
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RDW
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low MCV/nl RDW
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uncomplicated thalessemia
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low MCV/high RDW
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early Fe def anemia
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critical value- <50,000 or >1million, nl(140-400,000)
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platelets
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formed in bone marrow from megakaryocytes, role in hemostasis forming a plug to ensure vascular integrity
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platelets
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manual counts done on Neubauer hemocytometer. These are est as part of the differential
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platelets
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100 wbcs are counted and # represent a % is reported. RBC morph and platlet est also given
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differential
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red blood cells production in the
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bone marrow
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rbc controlled by erythropoietin (procrit) produced in the
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kidneys
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7-8um in size, biconcave disc, capable of altering shape, avg lifespan is 120dys, old/damaged recycled in spleen
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RBCs
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7-8 microns RBC
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normocytic RBC
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<7 microns, MCV <80, Fe def anemia, thalessemias, children
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microcytic RBC
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>8microns, MCV >101, liver disease, B12/folate def, newborns
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macrocytic RBC
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variation in shape of RBC
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poikilocytosis
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no central area of pallor, no biconcavity, MCHC>36%, osmotic fragility, can easily burst
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spherocyte-RBC morph
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breakdown of RBCs can develop gallstones, hereditary sperocytosis, hemolytic anmeia, ABO transfusion reactions
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spherocyte-RBC morph
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oval shaped RBC with white area in the center, hereditary ovalocytosis, sickle cell, Fe def, thal, megaloblastic anem
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ovalocytes - RBC morph
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small clump of Hgb in center surrounded by area of pallor, a thin rim of Hgb,
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target cells(leptocytes) rbcmor
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cells appear larger since it is flatter than nl, liver disease, thal, hemoglobinopathies, post-splenectomy
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target cells(leptocytes) rbcmor
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abnl hemoglobins, liver disease, thalassemias
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target cells(leptocytes) rbcmor
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hereditary conditions, some anemias
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elliptocytes -RBC morph
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sickle cell anemia (Hb SS), Hb SC, Hb S/thal
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sickle cells - RBC morph
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fragmented or pieces of cell, prosthetic heart valves
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schistocytes - RBC morph
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RBC with evenly placed blunt or rouned projections, more thorny projections
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burr cells (acanthocytes)
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severe liver disease, uremia, DIC, TTP, carcinoma. Anorexia, severe burns and hypothyroidism
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burr cells (acanthocytes)
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tennis racket, "pt crying for a bone marrow",fibrotic bone marrow, ineffective erythropoesis
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tear drop cells -rbc morph
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"smiley cells-slitlike areas of central pallor, liver disease, artifact, lupus
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stomatocytes-rbc morph
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bite cells, pac man, G6PD crisis, DIC, pulmonary emboli
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helmet cells-RBC
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RBC fragments found in severe burn pts, disseminated intravascular coagulation
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schistocytes - RBC morph
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spiked red cells are observed in liver disease, asplenic pts (spleens removed)
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acanthocytes
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red cells without a pale center are seen in hereditary spherocytosis, some immune-mediated hemolytic anemias
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spherocyte-RBC morph
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normochromia, hypochromia, polychromasia or hyperchromia, anisochromia
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hemoglobin content
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decreased hemoglobin concentration in pale cells
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hypochromic RBC
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nl area of central pallor should be about one third of the cell's diameter
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Nl red blood cells
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numerous dark purple dots throughout the RBC, Lead or heavy metal poisoning-blue/back gume lines
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basophilic stippling
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pale and filled cells can both be seen following blood transfusion
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Anisochromia
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small dark purple dot near RBC periphery, represent a DNA remnant, post splenectomy
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Howell-Jolly bodies
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pappenheimer bodies blue purple dots in sm groups in RBC, repres iron particles in the RBC
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siderocytes
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can be confirmed with Prussian blue reaction
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siderocytes
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denatured or percipitated protein seen in G6DP def, drug incuded hemolytic anemia
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Heinz Bodies
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stack of coins, due to abn proteins found in blood such as in multiple myeloma
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rouleaux formation
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last stage of dev prior to becoming a mature RBC, have reminant of RNA circulate for 24hrs,
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reticulocytes
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reflects responsiveness and potential of bone marrow (erythropoitic activity)
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reticulocytes
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they are suggested by basophilia or polychromasia on Wright's stain
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reticulocytes
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after adequate dosing of Fe supplementation for Fe def anemia, reteic may rise to >20% indicates
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good response to therapy
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reported count X pts HCT/nl HCT
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RI reticulocytes
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nl range .5-2% for adults 2.5-6.5% in newborns, .5-3.1 infants of tot RBCs
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RI reticulocytes
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measures the ability of the bone marrow to react to anemia and make RBCs
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Reticulocyte count
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monitors (5-7dys) response to anemia therapy
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Reticulocyte count
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is an immature RBC that still has some microsomal & ribosomal material detected with methylene blue
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reticulocyte
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1(this calculated by multiplying the retic count% X pt's HCT/nl HCT
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reticulocyte index
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the rate at which RBCs settle out of anticoagulated blood in one hr (mm/hr)
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erythrocyte sed rate
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inflammation and necrotic processes cause an alteration in blood proteins resulting in …(positive changes)
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aggregation of red cells
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the red cells become heavier and fall more rapidly leading to a …
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higher ESR
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nonspecific and non-dx and doesn't correlate directly to the severity of the disease
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ESR
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nl ranges by westergren method is men 0-15, women 0-20, kids 0-10 mm/hr
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ESR
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should not be performed on blood oler than 12 (4) hrs
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sed rates
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it is most useful with polymyalgia rheumatica and temporal arteritis
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ESR
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useful test to monitor inflammation (non cardio-specific CRP)
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C-reactive protein
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incr'd in infection, inflammation, multiple myeloma, macrocytic disorders, acute MI, pregnancy
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ESR (erythrocyte sed rate)
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dec'd in microcytic disorders, polycythemia vera, hereditary spherocytosis, sickle cell anemia, hemoglobin C disease
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ESR (erythrocyte sed rate)
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nl in allergies, viral infections, cirrhosis, malaria
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ESR (erythrocyte sed rate)
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5% daily requirement (20-25mg)-1mg newly absorbed (recycled), 2mg menstruating females
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iron def anemia
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stored as ferritin and hemosiderin (insoluble form)
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iron def anemia
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inc'd transferrin sythesis
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iron def anemia
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total iron binding capacity of transferrin TIBC
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iron def anemia
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dec'd % saturation (<15%)
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iron def anemia
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most common cause of microcytic anemia
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iron def anemia
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supply vs demand- neg Fe balance first detected by low ferritin (iron stores).
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iron def anemia
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when all stores are depleted then see dec serum Fe (bound) & inc TIBC (transferrin), %sat dec, anemia develops
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iron def anemia
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most common cause of Fe def in adults
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chronic blood loss(gi, menses)
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most common cause of Fe def in kids
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deficient diets
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symptoms fatigue, dypsnea on exertion, pica-hallmark, may crave ice or complain of a sore mouth
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iron def anemia
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signs- pallor, epithelial cell shedding-atrophic glossitis, cheilitis, spooning of nails
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iron def anemia
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lab- microcytic hypochromic anemia, inc RDW, retic monitors response to tx, ferritin, TIBC, serum Fe, %saturation
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iron def anemia
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tx-iron repalcement(slow Fe, feosol) given between meals, Colace better tolerable, constipation,
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iron def anemia
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consider transfusing pack RBCs if Hgb is <6 gms/dl
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iron def anemia
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cobalamin
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vit b12
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nl daily requirement 2-5 ug, stored in liver (1 ug/g liver tissue), ingested in meats, eggs, dairy products
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vit b12
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gastric acid and pepsin hydrolyze vit from protein which binds it
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vit b12
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atrophy of gastric mucosa (parietal cell) leads to lack of intrinsic factor and HCL secretion
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b12 pernicious anemia
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b12 needs for absorption
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intrinsic factor
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impaired DNA synt results in RBC with immature chromatin and appears enlarged or megaloblastic from nonabsorp b12
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b12 pernicious anemia
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average age 60yrs, fam history, associated with autoimmune diseases
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b12 pernicious anemia
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alcoholism, ascorbic acid, cimetedine (tagamet) oral contraceptives, strict vegens, gastric bypass
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b12 pernicious anemia
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MCV>95, dec'd retics, hypersegmented neutrophils, howell-jolly bodies (DNA remnant)
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pernicious anemia
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schillings test
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pernicious anemia
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tx- IM or SC B12 (byanocobalamin) once weekly for eight wks, then one monthly lifelong
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pernicious anemia
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meds(folic acid antagonists)-methotrexate, trimethoprim-sulfamethoxazole, triamterene
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folic acid def
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phenytoin and phenobarbital-interfere with intestinal absorption of folic acid
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folic acid def
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abnl synthesis of alpha or beta subunits of hemoglobin
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hemoglobinopathies
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sickle cell trait-substitution of valine for glutamate on beta chain
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hemoglobinopathies
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thalassemias-deficiency or absence of subunit, mediteranean ancestry
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hemoglobinopathies
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rigid, lifespan (20dys)
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sickle cells disease
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autosomal recessive, trait A/S 8-10% AA carry trait
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sickle cell disease
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inflexible rigid, inc viscosity, stasis, mech obstruction of sm arterioles leading to ischemia
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sickle cell
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occurs when deoxygenation is present due to vasoconstriction due to de temp or presence of acidotic state
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sickle cell
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painful swelling (hand-foot synd), delayed puberty, dactylitis, priapism
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sickle cell
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Hgb 5-11 gms/dl, normochromic, normocytic, inc retics, smear reveals sickle cells and nucleated RBCs
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sickle cell
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sodium metabisulfite reduction test -25%
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sickledix
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hemoglobin electrophoresis (gold std)
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sickle cell
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in disease all s and no A, trait will show S and A
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sickle cell
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tx hydroxyurea or butyrates will inc hemoglobin F, HLA compatible donors
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sickle cell
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hereditary hemoglobinopathies, defect prod of globin chains - alpha or beta
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thalassemia
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due to a deletion - SE asians, chinese, AA
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alpha thalessemias
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due to a gene mutation - mediterranean desent, chinese, asian, AA
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beta thalessemias
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@@/@@' B/B
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nl
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-@/-@' B/B
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alpha thal trait
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- - /@@'
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alpha thal minor
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--/--'
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alpha thal major
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bart's disease still birth
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alpha thal major
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--/-@
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Hgb H disease
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beta thalessemia major- cooley's anemia
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homozygous
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RDW nl as all RBCs are small no variation in size
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thalassemia
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RDW can help differentiate from Iron Def Anemia (IDA)
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thalassemia
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more anisocytosis, more variation, inc RDW
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iron def anemia
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hemoglobin electrophoresis- will see increased A2
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beta thalessemias
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acquired or genetic pancytopenia-dec in all cell lines due to dam to hematopoietic stem cells
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aplastic anemia
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may be due to toxic compounds, DDt, benzene, antibiotics, infections, hep, EBV, immuno changes graft vs host, pregnancy
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aplastic anemia
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CBC-pancytopenia, hematuria on UA, MCV >104, nl TIBC, dec retic, elevated erythropoietin levels, bone marrow biopsy
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aplastic anemia
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Fe overload due to inc'd Fe absorption in the gut, body can't exrete Fe and excess stored in liver, heart, pancreas. 20g<
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hemachromatosis
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genetic, ages 40-60, males to females 8:1, women lag due to menstruation
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hemachromatosis
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greatest risk if untreated is hepatomas
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hemachromatosis
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Fe usually stored as ferritin, now also deposited as hemosiderin
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hemachromatosis
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lab- ferritin> 300 ug/L men, >120 for women is dx, % sat>62% is confirm for homozygous state, def dx with liver biopsy
|
hemachromatosis
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tx-phlebotomies, one unit contains 250 mg of Fe, may need 80 phlebotomies initially, 2-4 yearly
|
hemachromatosis
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if induced by transfusions and is not hereditary then use chelating agents (tea aslo chelates Fe), screen fam members
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hemachromatosis
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incd CFU results in unregulated proliferation in absence of erythropoietin leading to inc'd blood viscosity and dec'd cerebral flow
|
Polycythemia Vera
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mean age 60, s/s h/a, tinnitis, "fullness in head and neck" epitaxis, pruritis after bathing is characteristic
|
Polycythemia Vera
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WBCs>12,000, inc'd RBCs, platelets>500,000, large bizarre forms, inc'd LAP, nl erythropoietin level
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Polycythemia Vera
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tx-phlebotomy to reduce symptoms, cytoreductive drugs (hydroxyurea or interferon. After"spent phase" terminates in leukemia
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Polycythemia Vera
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most common anemia seen in hospital pts
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anemia of chronic disease
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seen in pts with malignancies, diabetes, chronic inflamm disease, bacterial infections
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anemia of chronic disease
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caused by production of lactoferrin, a storage protein with greater affinity for Fe than transferrin
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anemia of chronic disease
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labs, hematocrits generally >25%, MCV is nl to low, nl RBC morph and retics, dec serum Fe, dec transferrin, inc ferritin
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anemia of chronic disease
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tx of primary disorder, don't give Fe supplementation as this can cause Fe overload
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anemia of chronic disease
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x-linked, more severe forms occur in Mediterranean and middle eastern men
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G6PD def
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RBC can not deal with oxidative changes damaged hemoglobin accumulates in RBC as heinz bodies, removed by spleen
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G6PD def
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oxidation and hemolysis occur when pt ingests oxidative drugs such as antimalarials, ASA, sulfa drugs
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G6PD def
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fava beans, febrile illness, or acidotic states can also cause a hemolytic crisis
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G6PD def
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s/s palpitations, SOB, dizziness, 1-3 dys after ingestion of an oxidant. Jaundice and splenomegaly common
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G6PD def
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labs- helmet and heinze bodies (special stain, assay G5DP levels
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G6PD def
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other cause of anemia- RBCs are fragmented by shear forces or turbulence, aortic stenosis, prosthetic heart valve
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mechanical hemolysis
|
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drugs act as haptens- bind to RBC membrane and induce synthesis of anti-drug antibodies
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drug induced anemia
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formation of immune complexes with immunoglobulins, fix complement-hemolysis
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drug induced anemia
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induced synthesis of Rh antibodies e.g. L-dopa and alpha methydopa, hemolysis may continue after d/c
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drug induced anemia
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anti-RBC IgG- (warm reacting antibodies) above 31 deg c, RBCs removed by spleen leading to anemia
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autoimmune hemolysis
|
|
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cold reaction antibodies (IgM) formed RBC complexes below 31 deg C can cause either hemolysis or agglutination of RBC
|
autoimmune hemolysis
|
|
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primary tx is avoidance of cold temp exposures
|
autoimmune hemolysis
|
|
|
dominantly inherited defect in RBC membrane proteins -result in spherical RBCs, function nl but get trapped and dest in spleen
|
hereditary spherocytosis
|
|
|
major finding is splenomegaly, may also see hepatomegaly and choleithiasis
|
hereditary spherocytosis
|
|
|
lab- spherocytes and reticulocytosis, negative Coomb's
|
hereditary spherocytosis
|
|
|
tx is splenectomy for severe anemias as this will stop emolysis, underlying defect is not changed
|
hereditary spherocytosis
|
|
|
classification-myeloid vs lymphoid, acute (immature cells) ALL, AML vs chronic (mature different cells) CLL, CML
|
leukemias
|
|
|
T or B cell, 80% or all childhood leukemias, peak ages 3-7, 80% B cell origin
|
acute lymph leukemia ALL
|
|
|
labs- WBC low to high, blasts, dec'd RBCs and platelets as bone marrow is taken over by lymphocytic cells
|
acute lymph leukemia ALL
|
|
|
tx- chemo, cure rate 50-60% in kids, 40% in adults, bone marrow transplant
|
acute lymph leukemia ALL
|
|
|
more common in adults, may see DIC, inc'd risk of infection due to neutropenia
|
acute myelogenous leuk, AML
|
|
|
labs- auer rods are pathognomic, bone marrow stains inc myelopreroxidase or paraminosalicylic acid
|
acute myelogenous leuk, AML
|
|
|
tx- chemo -relapse 12-18mnths, long term 15 yr survival) is only 10-15%
|
acute myelogenous leuk, AML
|
|
|
more mature myeloid cells rather than the blasts seen in AML
|
chronic myelogenous leuk, CML
|
|
|
younger middle aged adults
|
chronic myelogenous leuk, CML
|
|
|
philadelphia chromosomes- acuried translocation of chromosome 9 & 22, pathogenomic, presents in 95% of cases
|
chronic myelogenous leuk, CML
|
|
|
stable and then disease progresses to acute leukemia
|
chronic myelogenous leuk, CML
|
|
|
lab-inc'd WBCs (usually greater than 150,000/uL), dec'd or absent LAP (leukocyte alkaline phosphatase),
|
chronic myelogenous leuk, CML
|
|
|
southern blot tests for philadelphia chromosome
|
chronic myelogenous leuk, CML
|
|
|
tx-chemo and alpha-interferon for acute phase-palliative not curative, eventually progresses to blast crisis
|
chronic myelogenous leuk, CML
|
|
|
survival is 4 yrs after onset. Bone marrow transplant increases survival time but is rarely curative
|
chronic myelogenous leuk, CML
|
|
|
pt with infection or severe inflam disease have inc'd wbcs and blasts. This can be confused with CML
|
leukemoid reaction
|
|
|
has dec'd or absent LAP
|
chronic myelogenous leuk, CML
|
|
|
demonstrated an inc'd LAP
|
leukemoid reaction
|
|
|
may also be seen in polycythemia vera and third trimester pregnancy
|
inc'd LAP
|
|
|
neoplastic disorder of mature B cells (T cell types are very rare)
|
chronic lymphocytic leukemia
|
|
|
B cells don't differentiate into plasma cells and B cells create autoantibodies to RBCs and platelets
|
chronic lymphocytic leukemia
|
|
|
more common in men, older>50 with median age at dx is 65yrs, often asymptomatic
|
chronic lymphocytic leukemia
|
|
|
labs-inc'd WBc inc'd lymphs-more mature lymph is seen on smear, smudge cells are pathognomonic
|
chronic lymphocytic leukemia
|
|
|
tx- palliative, median survival is 6yrs, unlike CML, there is no blast crisis transforamtion to acute leukemia
|
chronic lymphocytic leukemia
|
|
|
b cells - fine hairlike projections
|
hairy cell leukemia
|
|
|
middle aged men
|
hairy cell leukemia
|
|
|
usually no adenopathy, all pts have splenomegaly
|
hairy cell leukemia
|
|
|
lab-pancytopenia (inc'd WBCs in 25%pts), hairy cell on smear, infiltration of red pulp on spleen (lymphomas infiltrate white pulp
|
hairy cell leukemia
|
|
|
tx- chemo with complete remission in 80% of pts, indolent course, survival is 10+ yrs
|
hairy cell leukemia
|
|
|
cancer of macrophage origin
|
hodgkin's lymphoma
|
|
|
bimodal distribution ages 20's and 50's
|
hodgkin's lymphoma
|
|
|
painless adenopathy (neck), night sweats, pruritis
|
hodgkin's lymphoma
|
|
|
labs-lymph node biopsy reveals Reed-Sternberg cells-lg multinucleated reticular cells-pathognomonic
|
hodgkin's lymphoma
|
|
|
tx-radiation and chemo-good prognosis, cure rates 80% even for stage III disease
|
hodgkin's lymphoma
|
|
|
single node - lymphoma staging
|
stage I
|
|
|
two or more nodes on same side of diaphragm - lymphoma staging
|
stage II
|
|
|
both sides of the diaphragm - lymphoma staging
|
stage III
|
|
|
involvement of extralymphatic organs, eg. Bone marrow, liver, lung - lymphoma staging
|
stage IV
|
|
|
neoplasm of lymphocytes
|
non-hodgkin's lymphoma
|
|
|
prognosis is poorer than for hodgkins disease
|
non-hodgkin's lymphoma
|
|
|
lab-smear can be nl, LDH inc if disease has spread. Dx is with lymph node biopsy
|
non-hodgkin's lymphoma
|
|
|
Tx is palliative, chemo, radiation
|
non-hodgkin's lymphoma
|
|
|
form of NHL affects B cells
|
burkitt's lymphoma
|
|
|
endemic in parts of Arfica, more common in kids and young adults
|
burkitt's lymphoma
|
|
|
US - abd pain and fullness
|
burkitt's lymphoma
|
|
|
Africa - jaw involvement
|
burkitt's lymphoma
|
|
|
assoc with chromosomal translocation of 8 and 14. African form is related to EBV
|
burkitt's lymphoma
|
|
|
neoplastic proliferation of plasma cells and monoclonal immunolobulin
|
multiple myeloma
|
|
|
affects men and women equally with peak incident 50-60 years old
|
multiple myeloma
|
|
|
monoclonal IgG more common than IgA
|
multiple myeloma
|
|
|
monoclonal kappa or lamda chains - bence jones proteins in urine
|
multiple myeloma
|
|
|
bone pain, pathologic fractures, bone marrow is preplaced with plasma cells, frequent infection with encapsulated organisms
|
multiple myeloma
|
|
|
lab-SPEP(serum protein electrophoresis) reveals paraproteins, abn plasma immunoglob, rouleaux form of RBC,
|
multiple myeloma
|
|
|
x-ray shows osteolytic bone lesions, hypercalcemia
|
multiple myeloma
|
|
|
inc'd b cell line, inc'd monoclonal IgM production
|
waldenstrom's macroglobulinemia
|
|
|
hyperviscosity
|
waldenstrom's macroglobulinemia
|
|
|
lab-rbc show rouleaux formation, bone marrow shows inc'd plasma cells, no osteolytic lesions, SPEP monoclonal IgM spike
|
waldenstrom's macroglobulinemia
|
|
|
tx-plasmapharesis to dec viscosity, chemo, survival 3-5 yrs from dx
|
waldenstrom's macroglobulinemia
|
|
|
neoplastic CD4 T cells
|
mycosis fungoides
|
|
|
infiltrates dermis and epidermis may involve lymph nodes and viscera
|
mycosis fungoides
|
|
|
can be confused with eczema and psoriasis
|
mycosis fungoides
|
|
|
dx with skin biopsy
|
mycosis fungoides
|
|
|
tx with topicals and phototherapy
|
mycosis fungoides
|
|
|
the process of blood development and production
|
hematopoiesis
|
|
|
all cells are produced from a multi-potential stem cell in the
|
bone marrow
|
|
|
granulocytes (phagocytes) and lymphocytes (recognition of non-self)
|
white blood cells
|
|
|
retain neutral stain and appear light tan
|
neutrophil
|
|
|
segs or polymorphonuclear cells - PMNs, "polys"
|
neutrophil
|
|
|
90% stored in bone marrow, adhere to endothelium
|
neutrophil
|
|
|
6-8hrs in circulation-migrate to tissues phagocytosis/apoptosis
|
neutrophil
|
|
|
the more mature, the more lobulations of the nuclei
|
neutrophil
|
|
|
the more mature forms of neutrophils are called
|
segs
|
|
|
the more immature forms of neutrophils are called
|
stabs or bands
|
|
|
left shift of neutrophils release of less mature forms and is def as when more than 12% bands are seen when tot PMN count
|
infect/inflammat/hemorrhage
|
|
|
-shift of neutrophils or hypersegmented can be seen in megaloblastic anemiaa and liver disease
|
right shift
|
|
|
inc'd in absolute # in response to invading organisms or tumor cells, kids respond to infect with higher degree than adults
|
neutrophilia
|
|
|
may be due to dec'd production excess stored in blood vessel margin, or too many called into action and used up
|
neutropenia
|
|
|
in interstinal mucosa and lungs in large numbers, allergies, parasitic infections, lower in morning, rise from noon to midnight
|
eosinophils
|
|
|
capable of phagocytosis (Ag-AB complexes) not bacterial -cidal
|
eosinophils
|
|
|
becomes active in later stages of inflammation
|
eosinophils
|
|
|
respond to allergic and parasitic conditions
|
eosinophils
|
|
|
counts are lower in the morning rise from noon until after midnight, nl 1-4%
|
eosinophils
|
|
|
NAACP-neoplasm, allergy, addison's disease, collagen, vasc disease, and parasites, PIE pulm infiltrate eosion
|
eosinophilia
|
|
|
due to inc'd adrenal steroids (cushing's), drugs- ACTH, epi, prostaglandins, stressful situations, burns, labor postop states
|
eosinopenia
|
|
|
small number in peripheral blood
|
basophils
|
|
|
long-lasting in blood with ciruclating lifespan of 2 wks
|
basophils
|
|
|
contain heparin, histamine, serotonin, and leukotriene B4
|
basophils
|
|
|
immediate and delayed hypersensitivity reactions
|
basophils
|
|
|
phagocytic basophils are called this when found in tissues
|
mast cells
|
|
|
nl .5-1%
|
basophils
|
|
|
CML, hodgkin's disease
|
basophilia
|
|
|
hyperthyroidism, acute phase of infection, stress
|
basopenia
|
|
|
leave circulation in 16-36hrs, enter tissues, mature into mascrophages
|
monocytes
|
|
|
present in lymph nodes, alveoli, spleen, liver, bone marrow
|
monocytes
|
|
|
APC antigen presenting cell/dendritic cells
|
monocytes
|
|
|
the largest cell of nl blood
|
monocytes
|
|
|
body's second line of defense against infection
|
monocytes
|
|
|
mobile via pseudopods, removed injured or dead cells, microorganisms, and insoluble particles from circulating blood
|
monocytes
|
|
|
monocytes migrate to the tissues where they become
|
macrophages
|
|
|
recovery state of acute infection, TB, subacute endocarditis
|
monocytosis
|
|
|
prednisone tx, RA, hairy cell leukemia
|
monocytopenia
|
|
|
t cells predominant, B cells, Nk cells (20-40%)
|
lymphocytes
|
|
|
not phagocytic but can be cytotoxic-complement activation, antibody dependent cellular cytotoxicity
|
lymphocytes
|
|
|
membrane markers CD ( clusters of differentiation)
|
lymphocytes
|
|
|
T cell CD4 or CD8 cell mediated immunity
|
lymphocytes
|
|
|
B cells CD 20 antibody production
|
lymphocytes
|
|
|
NK cells CD56 cytotoxic for virus - infected cells and cancer cells
|
lymphocytes
|
|
|
inverted or reversed diff-more lymphs than neutrophils(nl in a kid), ALL, CLL, viral infection
|
lymphocytosis
|
|
|
chemo, radiation, nl in 22% of pop
|
lymphopenia
|
|
|
found in infectious mono, CMV infection, viral hepatitis, toxoplasmosis
|
atypical lymphocytes
|
|
|
impt in hemostasis, may be nl in count but not in function
|
platelets
|
|
|
abn in funct can be assessed with bleeding time
|
platelets
|
|
|
sudden exercise, post trauma, post surgical, esp after splenectomy
|
thrombocytosis
|
|
|
ITP, TTP, DIC, burns, snakes and insect bites, marrow suppressants-chemo radiation, alcohol addiction
|
thrombocytopenia
|
|
|
chromosome 9 and 22
|
philadelphia chromosome
|
|
|
dec RBC, dec Hgb,
|
anemias
|
|
|
b12/folate def, drug induced marrow toxicity - MCV >100fl
|
macrocytic RBC
|
|
|
acute blood loss, hemolytic anemia, anemia of chronic disease MCV 81-99 FL
|
normocytic, normochromic
|
|
|
Fe def, anemia of chronic disease MCV<80 FL
|
microcytic RBC
|
|
|
vascular system, platelets, coagulation (fibrin forming system), fibrinolysis (clot degradation), all involved in maintaining
|
hemostasis
|
|
|
imbalance can result in excessive bleeding or thrombosis
|
hemostasis
|
|
|
involves consumption of platelets and coagulation factors
|
hemostasis
|
|
|
vascular system acts to prevent bleeding by
|
vasoconstriction
|
|
|
diversion of blood away from damaged area, contact activation of platelets, activation of the coagulation syst to form fibrin clot
|
vasoconstriction
|
|
|
induces aggreagation of platelts and also releases tissue thromboplastin, which initiates fibrin formation
|
ADP (granules
|
|
|
140,000-440,000/ul
|
platelets
|
|
|
counts<20,000/uL at risk for spontaneious bleeding, sites not severity predictable
|
platelets
|
|
|
automated counts more accurate, interruption of electrical impulses
|
platelets
|
|
|
HIT- 30% patients
|
platelets
|
|
|
inhibits enzyme cyclooxygenase, which blocks the formation of prostaglandins, preventing platelet aggregation
|
aspirin
|
|
|
irreversibly acetylates cyclooxygenase-lasts lifespan of platelet
|
ASA
|
|
|
will have inc'd Bleeding time 4-7 dys after ingestion
|
ASA
|
|
|
reversibly inhibit COO and inhibits aggregation as long as drug remains in plasma
|
NSAIDs
|
|
|
nl 7-11 FL
|
mean platelet volume
|
|
|
relationship between platelet size and count
|
MPV
|
|
|
assess disturbances of platelet production
|
MPV
|
|
|
high MPV at 6 mnths postinfarction predictor of
|
reinfarction
|
|
|
elevated in hyperthyroid patients
|
MPV
|
|
|
ypothyroid-high plateley counts and low
|
MPV
|
|
|
all factors are produced in the liver except factor VIII-produced by platelets
|
coagulation factors
|
|
|
VIII produced by
|
platelets
|
|
|
the end stage of both the intrinsic and extrinsic coagulation cascades, product meshes into platelet plug stabilizing it
|
fibrinogen
|
|
|
I-fibrinogen, II-prothrombin, III-tissue factor(thromboplastin), IV-Ca, V-proaccelerin, VII-stable factor, VIII-antihemophilic factor
|
coagulation factors
|
|
|
IX-christmas factor, X-stuart factor, XI plasma thromboplastin antecedent, XII hageman factor, XIII fibrin stabilizing factor
|
coagulation factors
|
|
|
measures the extrinsic factors that are vit k dependent-these factors are I,II,V,VII, and X
|
prothrombin time
|
|
|
PET protimes monitor oral anticoagulant therapy to
|
warfarin (coumadin)
|
|
|
acts as vit K antagonist thus inhibiting the synthesis of these clotting factors.
|
warfarin (coumadin)
|
|
|
for excessive warfarin therapy the antidote is
|
vitamin K
|
|
|
protimes are drawn in a tub that contains sodium citrate as anticoagulant
|
blue tube
|
|
|
specimens should not be older than 12hrs, some las will reject if more than 4hrs
|
prothrombin time
|
|
|
std the reuslts from lab to lab, regardless of reagents or methods used for testing, ranges 2-3
|
INR(internat NL ratio)
|
|
|
Alcohol, diarrhea/malabsorption, drugs with ASA, allopurinol
|
prolonged Prothrombin time
|
|
|
diet high in fat or leafy green veg, benadryl (diphenhydramine), OCPs
|
shorten Prothrombin time
|
|
|
meaures the intrinsic system
|
PTT(partial thromboplastin time
|
|
|
used to monitor heparin
|
PTT(partial thromboplastin time
|
|
|
immed short life, inactivates prothrombin fact 2, and prevent formation of thromboplastin
|
Heparin
|
|
|
Reverse heaprin effects with
|
protamine sulfate
|
|
|
products of X,D,E,Y usually cleared by macrophages, inhib conversion of fibrinogen to fibrin, can't stabilize clot and exer anticoag
|
fibrin split products
|
|
|
increased in DIC and thromboembolic conditions such as DVT, MI, PE, and hepatic dysfunction
|
FSP or FDP
|
|
|
false positive healthy women immediately before and during menstruation, cirrhosis, metastaic CA
|
FSP or FDP
|
|
|
nl (blue, green, or purple top)
|
fibrin D-dimers
|
|
|
is acted on by plasmin to produce D-dimer fragments
|
fibrin
|
|
|
increased iin DIC, PE, and DVT
|
fibrin D-dimers
|
|
|
most sensitive test for DIC
|
fibrin D-dimers
|
|
|
qualitative negative
|
fibrin D-dimers
|
|
|
quantitative<250 SI Units
|
fibrin D-dimers
|
|
|
protein usually associated with adv mailignancies/shock/sepsis, attack fib to interrupt clot form and only second att-no FDPs
|
primary fibrinolysins
|
|
|
(plasmin) occur nl in response to blood clotting and primarily work on fibrin=FDP
|
secondary fibrinolysins
|
|
|
adult 200-400ng/dl, newborn 125-300ng/dl, <100mg/dl will result in spontaneous bleeding
|
Fibrinogen-factor I
|
|
|
part of common pathway of coagulation cascade will affect PT and PTT
|
Fibrinogen Factor I
|
|
|
produced by liver, is an acute phase reactant protein. Sharp rises in tissue inflammation and necrosis
|
Fibrinogen Factor I
|
|
|
may see reduced levels in malnourished states, liver disease, and consumption coagulopathies
|
Fibrinogen Factor I
|
|
|
low levels with large volume blood transfusions as banked blood does not contain fibrinogen
|
Fibrinogen Factor I
|
|
|
inc'd with estrogen and BCP, dec'd with Depakote, androgens and dilantin
|
Fibrinogen Factor I
|
|
|
nl 8-12sec, 25-35sec, plasma sample +thrombin=clot
|
thrombin time
|
|
|
assesses only final phase of common pathway, thrombin acts on fibrinogen's conversion to fibrin clot
|
thrombin time
|
|
|
used to detect presence of heparin, dec'd fibrinogen, aids in evaluation of prolonged PTT
|
thrombin time
|
|
|
nl 18-22sec, variation of the Thrombin Time in which venom from a pit viper is used instead of thrombin
|
reptilase time
|
