AAB Hem/Coag online Flashcards
1,5,8-13 what group
fibrinogen
Fibrinogen 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 serum
1,5,8-13
fibrinogen group
2,7-9,10 what grop
Prothrombin
Which grp is vit K dependent…
What factors…
prothrombin
2,7-9,10
HMWK, PK
11,12 what group
All 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 extrinsic
1,2,5,10 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 intrinsic
1,2,5,10 common
inhibitor
Test that tests amt of time it takes for fibrinogen to convert to fibrin
thrombin time
thrombin helps convert
Thrombin reagent used in these two tests
TT, fibrinogen
TT ref
10-15 sec
Similar to PT
increased TT due to
A/hypo/dys-fibrinogenemia
Heparin
Uses up fibrinogen…
-FDPs
-Thrombolytic therapy
Test that tests fibrin clot formation by using Thrombin and plotting clot times w/1:10 std dilution
Plasma diluted 1:10, thrombin added, clot time noted, calibration curve gives concentration with mean value
fibrinogen
In testing fibrinogen, concentration is…. …. to clotting time
ref range
inversely proportional to clotting time, longer time means less fibrinogen
200-400mg/dL
Increased fibrinogen in these 4
inflammation/tissue death
heart attack
prego
birth CTRL
decreased fibrinogen in these 4
-DIC (excess plasmin breaks down fibrinogen)
-thrombolytic therapy/ -fibrinolysis(same as DIC)
liver dysfuction
hypofibrinogemia
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 def
factor 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 graphs 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, DVT
Pulmonary embolism
Arterial 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…
PLT CT…
PTT increased
PFA100/PLT agg abnormal
PLT ct normal
Condition thats recessive sexlinked; hemorragic;
F8 def with normal PLT function
Hemophilia A
Hemophilia A:
PTT..
PLT func…
PTT increased
-because factor 8 is in intrinsic
PLT 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 PTT, intrinsic
Only vWD has abnormal PLT function(adhesion)
Hem A only has factor def, PLTs ct/fnc ok
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…
F13
positive is clot dissolves because no F13
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 up
BT, PT, APTT: decreased, coag factors used up
FSP/Ddimer…pos
In Liver disease, all but…are decreased
all but F8
Liver disease is associated with markedly elevated plasma factor VIII (FVIII) levels, whereas the synthesis of many other coagulation factors and proteins is reduced.
Factor VIII is produced by endothelial cells and tends to be upregulated in cirrhosis, augmenting coagulation
In vit K def, what factors are decreased
2,7,9,10 vit k dependent
What diff liver from vit k def
F8 is increased in liver disease,
Lupus anticoagulant seen in…
ab against aPTT is…
SLE
antiphospholipid ab
aPTT reagent is a phospholipid
Lupus anticoag:
PTT…
rest are…
mixing study…
PTT is increased but rest are normal because PTT has phospholipid which lupus anticoag is an ab against
mixing study isn’t corrected
Hemotopoetic order
HSC, MPP, Common, CFU
Where does hemotopoeisis begin
yolk sac
order of hemotopoiesis organs
-yolk sac(fetus only)
-liver, spleen
-(BM adult only)
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 these two
Proerthyroblast, rubriblast
What cell comes after Pronormoblast/Proerthythroblast.. Two names
Basophlic
normoblast/erythroblast
Prorubricyte
Polychromotaphilic normoblast is also these two
Polychromotaphilic erythroblast
Rubricyte
Orthochromatic normoblast also these two
Orthochromatic erthythoblast
Metarubricyte
Retic is also
Polychromatic ertythrocyte
RBC also
ertythrocyte
RBC:
1.)Pro,
2.)Basophilic (blue, young)
3.)Polychromatophilic(blue, red)
4.)Orthochromatic(red)
…./…..
normoblast/erythroblast
Last nucleated red cell, NRBC called these two
orthochromatic normoblast, erythroblast
Metarubricyte
RBC
5.)Retic or
6.)RBC or
5.)polychromatic erythrocyte
6.)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.)Megakaryoblast
2.)Promegakaryocyte
3.)Megakaryocyte
4.)PLT
…
Largest cell in BM, can make 1000 PLTs
Megakaryocyte
Diff between mono and promono
chromatin is finer/lacy in promono, nucleus more round,oval in pro
Hmg A:
2…2…chains
4…
…ring with…
2 alpha, 2 beta
4 heme grps
protoporphyrin 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,epsilon
Gower2:alpha, epsilon
Portland:zeta,gamma
….
Hmg F chains
2 alpha
2 gamma
Adult Hmg and %
A 97-98
A2 2-3
F 1
2 polypedtide chains that is only seen in embryonic
epsilon, zeta
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 thats the lowest and in adults
delta
Type of EDTA used in hematoloby
Di-potassium
anticoag in Coagulation, ratio
3.2% citrated plasma
1:9
Cell ct calculation
cells x DIL x 10/#sqmm
Cause of granular slides, decreased RBC/HCT
increased 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
lipemia
increased WBC
Hmg S/C
Average size of cell
volume/cell
MCV
MCV NV, calculation
total volume of each cell
80-100fL
HCT/RBC x 10
Microcytic value
Macrocytic…
<80fL
>100mL
Average hmg/cell
MCH
MCH
NV..
calculation…
28-34pg
Hmg/RBC x 10
Total Hmg concentration in volume of/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…
WBCs
WBC x 100/nrbc +100
Besides NRBCS, what two things increase WBC
lrg PLT
lyse resistant RBC
Fragmented RBCs falsely increase….
PLTS
increased angle makes a …smear
decreased angle makes a … smear
increased angle=thicker
decreased =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 B
Eosin Y
Azure B is….
stains….
Eosin Y is…
stains…
Azure B is basic, stains acid
Eosin 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
ESR
W
M
W: 0-20
M: 0-15
4 causes of increased ESR
inflammation
increased plasma proteins
rouleaux
RA
Retic ct:
dye used…
disc…
NV…
NMB
Miller disc
0.5-1.5%
Corrected retic ct calculation,
corrects for HCT
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 dithionite
Pos: turbid
Neg=transparent
Stain used in hmg electrophoresis to visualize bands…
meansured with…
Ponceau stain
densitometer
A densitometer is a device that measures the degree of darkness (the optical density) of a photographic or semitransparent material or of a reflecting surface.
negatively charged electrode
cathode
positively charged electrode
anode
Cellulose 8.6 migration from slow/cathod to fast/anode
C, S, F, A
crawl, 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
positive in myeloblast but not lymphoblasts
MPO
myelo-peroxidase
Stains phospholipids, neutral fats, sterol
-primary, secondary granules
-brown/black
-AML vs ALL
postive in myeloblast but no lymphoblasts
Sudan Black B
SBB
Enzyme hydrolyze ester linkages and frees nahthol
-diazonium salt causes insoluble pigment
-myelogenous cells line
-AML vs ALL
Naphtyl AS-D
Chloroacetate esterase
positive in myeloblast not lymphoblasts
The 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 AML
myelomon vs mono
alpha naphyl esterase
α-Naphthyl acetate, in contrast to naphthol AS-D chloroacetate, reveals strong esterase activity in monocytes
Stains glycogen, magenta
-acute lymphoblastic leukemia is POS
distinguishing acute lymphocytic leukemia (ALL) and nonlymphocytic leukemia
PAS
periodic acid schiff
Periodic Acid Schiff (PAS) support distinguishing acute lymphocytic leukemia (ALL) and nonlymphocytic leukemia
The 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.
Distinguishes CML from leukomoid
-enzyme is in secondary granules of PMNs
-scored
Leukocyte ALP
Leukemoid reactions cause an increase in neutrophils, whereas CML increases granulocytes.
Patients 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).
LAP score NV…
Leukomoid, severe bacterial LAP…
vs
CML LAP…
NV 13-130
Leukomoid/bacterial increased
CML decreased
Patients 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
Terminal deoxynucleotidyl transferase (TdT) is a biochemical marker for acute lymphoblastic leukemia (ALL).
TdT POS leukemia
ALL
Lymphoblastic leukemia
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, hemosiderosis
decreased in IDA
BM aspirate take from … … in adults
illiac crest
Light scatter at 90 degree is…scatter
shows…
side, granularity
Light scatter at 180 degrees is…scatter
shows…
forward
particle size
Stain uses acid elution, citrate phosphate buffer;
eluates all hmg except F…
F resist acid elution and are…
Kleihauer Betke
pink
Test that denatures A but F are resistant
alkali denature HmgF
Denatured hmg inclusions of RBC;
supravital stain using NMB, can’t be stained with wrights
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 degration
biliverdin, bili-albumin, bili diglucurondie, urobilinogen, stercobili
extravascular
intra or extravascular hmg degration
free 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, not with oxygen
Deoxy
RBC NV:
size, MCV..
7-8 microns, 80-100 fL
Microcyte…
macrocyte…
microns, MCV…
micro <7, <80fL
macro>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
2 names for target
codocyte, leptocyte
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 vacuole
helmet 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 fragility
hereditary, ABO incompatibility
spherocytes
cell with slit like palor, reversible
artifact, increased lipid
hereditary, 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
PB stain: siderocyte; sideroblastic, thall
Pappenheimer bodies
RBC inclusion that doesn’t stain with wright, only NMB/supravital;
round mass near cell membrane, aggregated denatured hmg
G6PD 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 valine replaces glutamic acid in beta chain, 6th position
homozygous
sickle cell disease
In sickle cell disease, what replaces what in the beta chain in the 6th position
Valine replaces glutamic acid
Sickle cell disorder with many sickles, targets, and HJ bodies
Sickle cell disease, SS
Hmg-pathy heterozygous,
Valine replaces glutamic acid 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/hypo
bleeding, prego
decreased iron/ferritin
increased 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
D.latum
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
PNH
paroxymal 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, complement
pos DAT, Donath Landsteiner
PCH
Paroxymal cold hmg
HUS, TTP, DIC,
plasmodium,babesia
bartonella, 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 neutrophilia
leukomoid 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 pos
PAS neg
what cell…
myeloblast
PAS neg is CLL also
MPO, SBB, specific esterase neg
PAS pos
what cell
lymphoblast
But not in CLL with PAS
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 basophils
dry tap, Ph chromosome
CML
Lymphoma ass w/Reed Sternberg cell,
elderly/males
Hodgkins lymphoma
PLTs:
size…volume…
live…
NV…
2-4microns, 10fL
7-10days
150-450,000
Fragmented RBC affect on PLT
increase
clott/satellism affect on PLT
decrease
test that test PLT fnc, detects PLT plug, closure time
depends on PLT func, ct, activity
PFA 100
In PFA 100
abnormal 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
HIT
heparin 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 Soulier
only agg w/ristocetin:
Glanzmanns
storage pool disease; no granules
gray PLT syndrome
most common PLT disorder, inhibits thromboxane A2
aspirin
In sickle cell disease what position does valine replace glutamic
6th
Hageman is factor
12
Stable factor is also called…
Is factor…
TF…
VII
TF: III
Another name for warfarin, test that monitors it
Coumadin, PT
TdT POS..
ALL
Donath Landsteiner tests for
Ab…
Condition…
AntiP
PCH
Two plt disorders aggregates with everything except Ristocetin
vWD, BS
Plt disorder that doesn’t react with anything but Ristocetin
Glannsmann
Most abundant nucleated cell in bone marrow
Metamyelocytes
