AABHemOnline2.1.24 Flashcards
1,5,8-13 what group
fibrinogenFibrinogen group – factors 1, 5, 8, and 13. This group is called the fibrinogen group because thrombin activates all of these factors including fibrinogen. Maybe it should have been called the thrombin
Group not vit k dep, consumed in coagulation, not in serum1,5,8-13
fibrinogen group
2,7-9,10 what grop
Prothrombin
Which grp is vit K dependent…What factors…
prothrombin2,7-9,10
HMWK, PK11,12 what groupAll of these factors are involved in the initial phase of the intrinsic system activation.
contact group
Group that is not vit K dep, activates instrinsic pathway, includes HMWK, 11,12
contact group
Intrinsic and common tested with what test
APTT
factors in intrisic pathway
8,9-11,12
Factors in extrinsic pathyway
7, 3(TF)
Extrinsic and common pathway tested with
PT/INR
factors in common pathway
1,2,5,10
factor not part of coag pathways and doesn’t affect testing
13
what does PT/PTT test for
crosslinked fibrin clot
I
fibrinogen
II
Prothrombin
III
Tissue thromboplastin, TF
IV
calcium
V
labile
VII
stable
VIII
antihemophiliac A
IX
antihemophiliac B
XI
anti hemophiliac C
X
Stuart Prower
XII
Hageman
XIII
fibrin stabilizing
inactive form of plasmin
plasminogen
fibrinolysis is breakdown of fibrin by act of
plasmin
insoluble fibrin breaks down to
D-dimer
soluble fibrin breaks down to
FDPs
Thromboplastin (TF, Ca) used in
PT
ISI is used to calculate the INR for the…
PT
Test that monitors wafarin/coumadin
PT
Two methods for PT, PTT, TT
optical and electromechanical
PT ref range
10-13sec
Increased PT associated with factors…
7 extrinsic1,2,5,10 common
Activated partial thromboplastin reagent in aPTT is a
phospholipid
Two reagents in aPTT
activated partial thromboplastin/phospholipid and CaCL
PTT range
30-36sec
Increased aPTT associated with factors…and also this….
8,9,11,12 intrinsic1,2,5,10 commoninhibitor
Test that tests amt of time it takes for fibrinogen to convert to fibrin
thrombin time
Thrombin reagent used in these two tests
TT, fibrinogen
TT ref
10-15 secSimilar to PT
increased TT due to
A/hypo/dys-fibrinogenemiaHeparinFDPsThrombolytic therapy
Test that tests fibrin clot formation by using Thrombin and plotting clot times w/1:10 std dilution
fibrinogen
In testing fibrinogen, concentration is…. …. to clotting timeref range
inversely proportional to clotting time, longer time means less fibrinogen200-400mg/dL
Increased fibrinogen in these 3
inflammationpregobirth CTRL
decreased fibrinogen in these 3
DICliver dysfuctionhypofibrinogemia
Test that differentiates factor def from lupus inhibitor using 1:2 dilution of PT plasmsa to normal pooled plasma running PT/APTT
mixing study
If PT/PTT is correct in a mixing study, this indicates a…follow up with a … …
factor deffactor assay
If PT/PTT is not corrected with mixing study,indicated an….
inhibitor
Factor assay normal range
50-100% activity
Test where you do PT,APTT and get std curve from dilutions; times are converted to % activity
factor assay
Factory assay should be…
linear
Nonlinear in a factor assay indicates
inhibitor
Test which uses monoclonal ab to detect fragments
D dimer
D dimer ref
<=0.50mg/mL
Increased Ddimer in these 4
DIC, DVTPulmonary embolismArterial thromboembolism
Test that tests for soluble fibrinogen, FDP with latex agglutination
FDP/FSP/fibrin monomer
Most common coagulation disorder, autosomal dominant disease
vWD
vWD lacks
F8:vWD
vWD:PTT…PFA100/PLT agg…
PTT increasedPFA100/PLT agg abnormal
Condition thats recessive sexlinked; hemorragic;F8 def with normal PLT function
Hemophilia A
Hemophilia A:PTT..PLT func…
PTT increasedPLT func normal
What do vWD and Hemophilia A have in common…How do you diff between vWD and Hemophilia A:
Both have F8 def and have increased PTTOnly vWD has abnormal PLT function
Recessive, sexlinked F9 def
Hemophilia B
autosomal recessive F11 def
Hemophilia C
Def that is part of common pathway where both PT and PTT is increased
fibrinogen def
Term when fibrinogen levels are below analytical range
A-fibrinogenemia
Term where fibrinogen is <200
Hypo-fibrinogenemia
Term where amt of fibrinogen is normal but PT/PTT are increased
Dys-fibrinogenemia
Factor def where all tests will be normal because it’s not part of coag pathway
F13 def
5M urea solubility test uses urea to dissolve clot, which def is tested using this…positive…
F13positive is clot dissolves
Def thats part of intrinsic, theres no history of bleeding and only the PTT is abnormal
F12 def
Disorde where theres formation of microthrombi followed by systemic fibrinolysis
Disseminated Intravascular coagulation
DIC:PLT ct, fibrinogen..BT, PT, APTT..FSP/Ddimer…
PLT ct, fibrinogen: decreased, all used upBT, PT, APTT: decreased, coag factors used upFSP/Ddimer…pos
In Liver disease, all but…are decreased
all but F8
In vit K def, what factors are decreased
2,7,9,10 vit k dependent
What diff liver from vit k def
F8
Lupus anticoagulant seen in…ab against aPTT is…
SLEantiphospholipid ab
Lupus anticoag:PTT…rest are…mixing study…
PTT is increased but rest are normalmixing study isn’t corrected
Hemotopoetic order
HSC, MPP, Common, CFU
Where does hemotopoeisis begin
yolk sac
order of hemotopoiesis organs
yolk sac, liver, spleen, BM
Medullary/BM/red marrow production of cells in adults in …bones of … and …
flat bones of illiac crest and sternum
extramedullary production of cells in adult are… and ….
liver and spleen
Pronormoblast is called
Proerthyroblast
What cell comes after Pronormoblast/Proerthythroblast
Basophlic normoblast/erythroblast
Polychromotaphilic normoblast is also
Polychromotaphilic erythroblast
Orthochromatic normoblast also
Orthochromatic erthythoblast
Retic is also
Polychromatic ertythrocyte
RBC also
ertythrocyte
RBC:1.)Pro, 2.)Basophilic, 3.)Polychromatophilic 4.)Orthochromatic…./…..
normoblast/erythroblast
Last nucleated red cell, NRBC called these two
orthochromatic normoblast, erythroblast
RBC5.)Retic or6.)RBC or
5.)polychromatic erythrocyte6.)erythrocyte
Retic called
polychromatic erythrocyte
Myeloid cell with red, azurphilic primary granules
Promyeloctye
Myeloid with 50% nucleus and specific granules
myelocyte
Lymphoid cell that one large prominent nucleoli
prolymphocyte
1.)Megakaryoblast2.)Promegakaryocyte3.)Megakaryocyte4.)PLT
…
Largest cell in BM, can make 1000 PLTs
Megakaryocyte
Diff between mono and promono
chromatin is finer/lacy in promono
Hmg:2…2…chains4……ring with…
2 alpha, 2 beta4 heme grpsprotoporphyrin ring w/iron
3 embroyonic hmg
Gower 1,2,Portland
2 zeta, 2 epsilon
gower 1
2 zeta, 2 gamma
Portland
2 alpha, 2 epsilon
Gower 2
Gower 1: zeta,epsilonGower2:alpha, epsilonPortland:zeta,gamma
….
Hmg F chains
2 alpha2 gamma
Adult Hmg and %
A 97-98A2 2-3F 1
polypedtide chain that is only seen in embryonic
epsilon
polypeptide chain thats in both fetal and adult, curve will have sharp incline before birth and be dominant in adult
alpha (hmg A,F)
Chain with curve that rises early before birth then decreases after birth
gamma
chain with curve at minimal rise until right after birth into adult
gamma
chain with curve thats the lowest and in adults
delta
Type of EDTA used in hematoloby
Di-potassium
anticoag in Coagulation, ratio
3.2% citrated plasma1:9
Cell ct calculation
cells x DIL x 10/#sqmm
Cause of granular slides, decreased RBC/HCTincreased MCV/MCHC
cold agg
Hmg concentration uses this method
cyan methmg
Cyan methmg measures all hmg except
Sulf-hmg
3 things that falsely affect Hmg
lipemiaincreased WBCHmg S/C
Average size of cellvolume/cell
MCV
MCV NV, calculation
80-100fLHCT/RBC x 10
Microcytic valueMacrocytic…
<80fL>100mL
Average hmg/cell
MCH
MCHNV, calculation
28-34pgHmg/RBC x 10
Hmg concentration/cell
MCHC
MCHC NV, calculation
32-36 g/dL, %Hmg/HCT x 100
hypochromic….hyperchromic…
<32>36 %
degree of anisocytosis
RDW
RDW NV, aniso
12-15>15
NRBCs falsey increase…correction calculation…
WBCsWBC x 100/nrbc +100
Besides NRBCS, what two things increase WBC
lrg PLTlyse resistant RBC
Fragmented RBCs falsely increase….
PLTS
increased angle makes a …smeardecreased angle makes a … smear
increased angle=thickerdecreased =thinner
small drop or big angle could cause a
short smear
big drop, sml angle could cause a
long smear
crenated smear due to
not dried throughly
Wright, Giesma are what kind of stains
Romanowsky
Two reagents in Romanowsky stain
Azure BEosin Y
Azure B is….stains….Eosin Y is…stains…
Azure B is basic, stains acidEosin Y is acidic, stains basic
Buffer to acidic, not enough staining, too much rinsing leads to
excessive pink and light staining
Buffer too alkaline, prolonged staining, not rinsing well leads to
excessive blue and dark staining
ESRWM
W: 0-20M: 0-15
4 causes of increased ESR
inflammationincreased plasma proteinsrouleauxRA
Retic ct:dye used…disc…NV…
NMBMiller disc0.5-1.5%
Corrected retic ct calculation
Retic ct x PT HCT/45%
RPI:uses PT HCT, normal HCT, Retic ct and is over 2 days
PT HCT/45% x retic ct/2 days
screen for HmgS, uses EDTA, Dithionite, doesn’t differentiate
Solubility test
Hmg S is insoluble in… …Pos solubility test versus neg
Hmg S insoluble in sodium dithionitePos: turbidNeg=transparent
Stain used in hmg electrophoresis to visualize bands…meansured with…
Ponceau staindensitometer
Cellulose 8.6 migration from slow/cathod to fast/anode
C, S, F, Acrawl, slow, fast, accelarated
Slowest/cathode to fastest/anode in citrate 6.2
-FASC+
Citrate 6.2 slow/cathode to fast/anode migration
F, A, S, C
Stain catalyzes oxidation of substance by H2O2-enzyme in primary granules-specific for granulocytes-diff AML from ALL
MPOmyeloperoxidase
Stains phospholipids, neutral fats, sterol-primary, secondary granules-brown/black-AML vs ALL
Sudan Black BSBB
Enzyme hydrolyze ester linkages and frees nahthol-diazonium salt causes insoluble pigment-myelogenous cells line-AML vs ALL
Naphtyl AS-D Chloroacetate esteraseThe aim of this stain is to demonstrate the presence of granulocytes. Granulocyte lysozomes contain a rather specific hydrolase that can use the Naphtol AS-D Chloroacetate as substrate. The liberated naphtol reacts with the diazonium salt “Fast Red Violet LB”, forming red depots.
Esterase in mons/macrophages, distinguishes AMML vs AMLmyelomon vs mono
alpha naphyl esterase
Stains glycogen, magenta-mature granulocytes, monos are posdistinguishing acute lymphocytic leukemia (ALL) and nonlymphocytic leukemia
PASperiodic acid schiff Periodic Acid Schiff (PAS) support distinguishing acute lymphocytic leukemia (ALL) and nonlymphocytic leukemiaThe periodic acid-Schiff (PAS) staining procedure is most commonly used in the histology laboratory to detect glycogen deposits in the liver when glycogen storage disease is suspected.
Distinguished CML from leukomoid-enzyme is in secondary granules of PMNs-scored
Leukocyte ALP
LAP score NV…Leukomoid, severe bacterial LAP…vsCML LAP…
NV 13-130Leukomoid/bacterial increasedCML decreasedPatients with leukemoid leukocytosis show very high LAP score due to high cytoplasmic alkaline phosphatase activity. On the other hand, in patients with CML, the neutrophils show a very weak reaction to the alkaline phosphatase staining (low LAP score).
TdT
Terminal Deoxynucleotidyl Transferase
TdT diff…from…
ALL from lymphoma
Stain that is nonvital, stains iron in BM
Prussian blue
Prussian blue increased iron staining in these 3, decreased in 1
increased in sidero,hemachromatosis, hemosiderosisdecreased in IDA
BM aspirate take from… …in adults
illiac crest
Light scatter at 90 degree is…scattershows…
side, granularity
Light scatter at 180 degrees is…scattershows…
forwardparticle size
Stain uses acid elution, citrate phosphate buffer; eluates all hmg except F…F resist acid elution and are…
Kleihauer Betkepink
Test that denatures A but F are resistant
alkali denature HmgF
Denatured hmg inclusions of RBC; supravital stain using NMB
Heinz body
Test using buffered NaCl with increasing hypotonic slns; amt of hemolysis measures spectrophotometrically
Osmotic fragility test
osmotic fragility test:NV…increased fragility…seen in…
NV 50%fragility <50%spherocytosis
Screen for PNH, using low ionic strength sln
sugar H2O
Test for PCH, antiP
Donath Landsteiner
Intra or extravascular hmg degrationbiliverdin, bili-albumin, bili diglucurondie, urobilinogen, stercobili
extravascular
intra or extravascular hmg degrationfree hmg, haptoglobin, methmg, urine hemosideran, heme/Fe, hemopexin
Intravascular
Hmg in ferrous state, Fe3+
oxyhmg
hmg oxidized to ferric state Fe2+
methmg
hmg with carbon monoxide
carboxy hmg
hmg and CO2
Deoxy
RBC NV:size, MCV..
7-8 microns, 80-100 fL
Microcyte…macrocyte…microns, MCV…
micro <7, <80fLmacro>8, >100fL
Cell with irregular thorn projections/sml bulblike tips; altered lipid content
acanthocytes
another name for acanthocytes
spur
cell with bulls eye, increased membrane lipids; decreased hmg, seen in hmg-pathies
targets
another name for target
codocyte
crescent, pointed end cell; polymerises into rods of descreased O2 tension; inhibits rouleux
sickle cell
another name for sickle cell
drepanocyte
cell with regular projections, reversible/article or liver disease
echinocyte
another name for echinocyte
burr
cell pencil/cigar to oval; hereditary, IDA, thall
elliptocytes, ovalcytes
cell with ecentric vacuole…this cell bursts and becomes…seen in HA, heart vaulve hem
blister has ecentric vacuolehelmet burst blister
another name for helmet
keratocyte
cell due to mechanical damage, hemolyze or removed by spleen; fibrin formation caused; TTP,DIC, burns
shistocyte
cell with MCHC >36, lost biconcave/no CP; increased osmotic fragilityhereditary, ABO incompatibility
spherocytes
cell with slit like palor, reversibleartifact, increased lipidhereditary, alcoholic, rhnull,lead
stomatocyte
cell with RBCs inclusions that go thru spleen than elongated, seen in thall/myelofibrosis
tear drop
another name for tear drop
dacrocyte
RBC inclusion with blue black evenly distributed coarse to fine granules;seen in lead/thall/hmg-pathies
basophilic stippling
RBC inclusion red/violet figure 8; remnants of mitotic spindle fibers; severse anema
cabbot ring
RBc inclusion that’s usually one dark purple spherical granule of DNA; post splenectomy, megablastic, HA
Howell jolly bodies
RBC inclusion in sml clusters of iron granules seen in wright or PB stain; sideroblastic, thall
Pappenheimer bodies
RBC inclusion that doesn’t stain with wright, only NMB/supravital;round mass near cell membrane, aggregated denatured hmgG6PD def, drugs, post splenectomy
Heinz bodies
RBC disorder with amino substituion
Hmg-pathies
RBC disorder with decreased production of globin chain
Thall
RBC disorder with decreased RBC etc
anemia
Hmg-pathy where glutamic acid replaces valine in beta chain, 6th positionhomozygous
sickle cell disease
In sickle cell disease, what replaces what in the beta chain in the 6th position
glutamic acid replaces valine
Sickle cell disorder with many sickles, targets, and HJ bodies
Sickle cell disease, SS
Hmg-pathy heterozygous,glutamic acid replaces valine in beta chain;mostly targets
sickle cell trait
Hmg-pathy with targets, crytals that look like washington monuments; polychromatophilia
Hmg C disease
Hmg-pathy with glove like cells, sickle, targets
Hmg SC
Thallesemia also called Cooleys anemia, micro/hypo; targets, baso stipling,less A, more A2/F
Beta Thall major
Hmg disorder where >2% Hmg F; hypoxia
hereditary persistance HmgF
Anemia secondary to disease, iron therapy doesn’t help; can be normo/normo to micro/hypo;storage iron/ferritin increases over time,iron/transferrin/hmg decrease
anemia of chronic
anemia with micro/hypobleeding, pregodecreased iron/ferritinincreased transferrin/TIBC
IDA
anemia thats micro/hypo, increased iron; pappenheimer bodies in wrights, siderocytes in PB, ringed sideroblasts in BM
siderblastic anemia
Cause of pernicious anemia due to def that affects DNA; macrocytes, hyperseg, megaloblastic
folic acid def
def that caused pernicious anemia due to lack of IF, can’t absorb B12 for DNA;macro, hyperseg
Vit B12 def
anemia with pancytopenia, hypocellular BM; drugs/chemo
aplastic anemia
Membrane defect, enzyme defect, immune and nonimmune are all causes of
HA
membrane defect where mchc >36, increased osmotic fragility
hereditary spherocytosis
membrane defect causing hemolysis and occurs at night; testing with sugar H2O, sucrose, HAMs
PNHparoxymal nocturnal hmglobinuria
Ezyme def that causes HA, cant reduce iron from ferric to ferrous;-seen in antimalarial drugs/fava beans-Heinz bodies
G6PD def
Cold agglutin disease, paroxymal cold hmg, warm auto are all
auto immune HA
HDN, hemolytic trans rxn, delay trans rxn are all
alloimmune HA
HA where RBC/HCT is decreased,MCV/MCH/MCHC all increased
cold agg
Immune HA where cold auto anti-P, biphasic, complementpos DAT, Donath Landsteiner
PCHParoxymal cold hmg
HUS, TTP, DIC, plasmodium,babesiabartonella, clostridium can all cause
nonimune HA
conditon with increased RBC/erythropoeitin; all cells increased;
polycythemia vera
cell with 3-5 lobes, many secondary granules
neutrophil
cell with 2-3 lobes, eosin specific granules
Eos
cell with large dark granules with heparine and histamine
Baso
Largest cell in blood, horseshoe nucleus/convoluted; lacy chromatin, ground glass vacuoles
mono
cell nucleus size of RBC, nucleus 90% of cell, condensed chromatin, no nucleoli
lymph
cell with convoluted light blue, abundant cyto, azurophilic granules
large granular lymph
cell with ecentric nucleus, coarse chromatin; deep basophillic cyto w/halo of golgi apparatus
plasma cell
WBC inclusion that are stacks of rough endoplasmic reticulum; light blue, single/multiple;seen in severse bacterial infections
Dohle bodies
WBC inclusion that are large blue black primary nonspecific granules;bacterial infections and leukomoid rxns
toxic granulation
WBC inclusions that make clear spots in cyto; seen in bacterial and leukomoid rxn
cytoplasmic vacuolozation
WBC inclusion seen in AML, red/blue needle in cyto
auer rod
Two conditions with increased WBC, left shift, Dohle bodies, vacuolization and due to severe bacterial infections
reactive neutrophilialeukomoid rxn
LAP is… in leukomoid rxn
LAP is increased
anomoly with hyposegmented segs
pelger huet
anomoly with azurophilic granules resembling toxic granulation; mucopolyssaccharides
Alder-Reily anomaly
anomaly with membrane defect of lysosomes, giant abnormal granules;albinism/photophobia
Chediak-Higashi anomaly
Anomaly with dohle bodies, giant PLTs, but decreased PLTs
May Hegglin
Gaucher, Tay Sachs, Nieman Pick, Fabrys are all
lipid storage diseases w/enzyme def, decreased monos
caused by EBV, saliva;10% reactive lymphs, increased WBCs
infectious mononucleosis
virus spread thru saliva/transfusion;increased WBC, reactive lymphs, negative monospot
CMV
condition with increased lymphs, negative monospot seen mostly in kids <5yrs of age
infectious lymphoctytosis
Leukemia affects young, sudden, >20% blasts in BM or blood; can have auer rods;MPO/specific esterase pos
AML
MPO, SBB, specific esterase posPAS negwhat cell…
myeloblast
MPO, SBB, specific esterase negPAS poswhat cell
lymphoblast
AML classifications…M0M1M2
M0 minimallyM1 noM2 maturation
L1 is what leukemia
childhood, TdT
L2 is what leukemia
adult T cell
L3 is what leukemia
burkitts,EBV, CALLA, poor prognosis
Leukemia in 60yrs older etc, many small mature lymphs/soccer ball, smudge cells
CLL
Leukemia in 50yrs older, TRAP pos, mononuclear w/hairlike
hairy cell
leukemia in older males, large bizarre cells with cerebriform nuclei
Sezary
leukemia in older, myeloid, decreased LAP, many basophilsdry tap, Ph chromosome
CML
Lymphoma ass w/Reed Sternberg cell,elderly/males
Hodgkins lymphoma
PLTs:size…volume…live…NV…
2-4microns, 10fL7-10days150-450,000
Fragmented RBC affect on PLT
increase
clott/satellism affect on PLT
decrease
test that test PLT fnc, detects PLT plug, closure timedepends on PLT func, ct, activity
PFA 100
In PFA 100abnormal collagen/epi indicates
aspirin
In PFA 100 abnormal collagen/epi/ADP indicates
vWD
ADAMTS13 def seen in
TTP
due to ab made to heparin/PF4 complex, PLTs are sensitized and cleared by spleen, decreased PLTs
HITheparin induced thrombocytopenia
syndrome with giant PLTs, abnormal PLT aggregation with ristocetin
Bernard Soulier syndrome
Quantitative PLT disorder with decreased giant PLTs and Dohle like bodies
May Hegglin
PLT aggregation disorder w/ristocetin, glycoprotein 2b/3a defect
Glanzmanns thrombasthenia
PLT adhesion issue, abnormal ristocetin
vWD
Two PLT disorders that are abnormal with ristocetin…One that only aggregates with ristocetin…
abnormal ristocetin:-vWD, Bernard Soulieronly agg w/ristocetin:Glanzmanns
storage pool disease; no granules
gray PLT syndrome
most common PLT disorder, inhibits thromboxane A2
aspirin
