fall heme week 1

proficiency testing is done on

whole blood, lyophilized serum/plasma, prepared slides and or digital images

hemolyzed specimen

dilutional effect on analytes, false increase of analytes, decreased erthrocyte counts

failure to mix with anti coag

clotted specimen and falsely decreased cell counts or prolonged coag test results

failure to follow order of draw

cross contaimination with collection tube additives

time of draw and patient anxiety or crying

analyte dependent (hgb highest in morning, increases leuk count)

over/under anticoag

<90% of expected vol= over anticoag, hct >55% = less plasma, over coag

daily QC requirements per CLIA

2 levels of quantitative, pos and neg qualitative, coag tests every 8 hrs

bulls testing algorithm calculates

moving average of each group pf 20 patient specimen using rbc indice precision and accuracy, X-B analysis

bulls testing algorithm range

determine rbc indicies on 500 consecutive patient specimens, plus or minus 3% of the mean for each

bulls testing algorithm unacceptable

review population of previous 20 specimen, if true alert instrument affecting one or more rbc parameter

analyzers automatically

evaluates numerical data and histograms, generates suspect flags for interfering substances, abnormal cell morph and cells

correction formula for proper vol of anticoag if hct over 55%

(1.85 × 10 -3) (100 - 63) V

cause elevation of hgb

lipemia, icterus, or hemolysis in plasma effecting MCH and MCHC, rule of 3

corrected hgb calculation

aliquot of well mixed blood, centrifuged, original hgb- supernatant hgb= hgb, recalculate mch and mchc

saline replacement

plasma removed from centrifuge specimen, replaced with equal vol of saline, specimen mixed and rerun for Hgb concentration

effect of cold agglutinins

decreased rbc count, increased mcv, decreased hct due to mcv, increased mchc > 36, fix by warming blood to 37 for 15

hemolysis interference

thromboplastin like substance released causing shortened clotting

lipemia or icterus

affects endpoint detection on photo-optical analyzers, use electromechanical or mechanical clot detection methods

anemia

decreased O2 carrying capacity of blood causing tissue hypoxia, decrease in hgb and or rbc concentration, signals underlying disorder, hgb/hct

anemia develops when

destruction exceeds marrow capacity or impaired production, marrow can compensate up to 5-8x normal output

erythrocyte kinetics

mass= production x survival, rbc lifespan= 100-120 days

hypervolemia and hypo

hyper- high plasma falsely low hgb/hct

hypo- low plasma, falsely high or normal hgb/hct

acute blood loss

initially normal hgb (rbc mass and plasma vol drop together), falls as plasma re-expands

acute loss values

20%- tolerated at rest

30-40%= shock

50%= death

if chronic functional 50% below normal

pallor

conjunctiva, nailbed, palm, tongue

jaundice and dark urine

indicates hemolytic process

koilonychia

iron deficiency

smooth tongue

megaloblastic anemia

bone deformities/expansion in children

chronic severe hemolytic anemia

bilirubin

hgb catabolism

urine and stool

occult blood, urobilinogen

micro/hypo

defective hgb synthesis, iron, thalassemia, chronic disease, sideroblastic

macro

impaired dna synthesis (B12/folate) or reticulocytosis

absolute retic count

% of retics x rbc

ref= 25-75 × 10 3

corrected retic % for anemia severity

% of retics x (patient hct/normal hct)

usually 45% hct used

reticulocyte production index RPI

corrected retic % / maturation time, the lower the hct the earlier retics were released from bm needing longer maturation time

reticulocyte production index RPI ref

>2= good, or survival defect/blood loss

<2= proliferation or maturation defect

immature reticulocyte fraction IRF

high rna content, earliest sign of marrow response, used for bm transplant or rHyEPO/iron therapy, better than RPI

reticulocyte hgb (CHr/RET-He)

hgb content of circulating reticulocytes, reflects iron available over the last several days, early indicator of iron therapy response

proliferation defect

low production, norm/norm, low retic, RPI<2

maturation defect

ineffective erythropoiesis, nuclear (megaloblastic), cytoplasmic (hgb synthesis)

survival defect

high loss, high retics, high IRF, RPI >2

compensated hemolytic disease

marrow keeps pace, no anemia

intrinsic hemolysis

hereditary, membrane, enzyme, or hgb defects, extravascular

extrinsic hemolysis

aquired, ab, mechanical, chemical, or infectious injury, DAT for immune mediated destruction, extra or intravascular

intravascular hemolysis

in circulation, complement activation, mechanical trauma, toxic microenvironment, low haptoglobin= hemoglobinemia, hemogloburia, hemosiderinuria, VERY high LDH

extravascular hemolysis

in spleen, liver, bm by macrophage phagocytosis caused by ab/complement coated or damaged rbc, high indirect bilirubin, urine/fecal urobilinogen, expired CO, and LDH, more common

serum bilirubin unconjugated test

from hgb catabolism, <4 even with active hemolysis

haptoglobin and hemopexin test

consumed clearing free hgb/heme, both decrease with hemolysis

LDH test

released from lysed cells, most elevated in intravascular hemolysis

urine hemosuderin and urobilinogen test

reflect hgb catabolism products

erythrocyte survival studies test

rarely used, localizes site of destruction in mild hemolysis

bm evaluation test

not routine, unless inconclusive workups

homogeneous vs heterogeneous

homo- normal rdw, hypoproliferative anemias, chrinic disease, some hemoglobinopathies

hetero- high rdw, nutrition def, iron def, dimorphic pop, uncompensated hemolysis

bm evatuation

indicate stem cell defect, marrow damage/replacement, inconclusive anemia, myeloid:erythroid ratio 1.5-3.3

low vs high M:E

low= hyperplasia, hemolytic anemia (marrow compensating)

high= proliferation defect (aplastic, infiltrative, chronic disease)

screening tests

high sensitivity, pos when disease is present (CBC, retic count)

reflex testing

one result guides the next

anemia testing path

CBC, RPI, morph/iron studies/B12 folate, confirm with smear or bm