AAB Hem/Coag online Flashcards by Leah McAleer

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

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Group not vit k dep, consumed in coagulation, not in serum

1,5,8-13

fibrinogen group

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2,7-9,10 what grop

Prothrombin

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Which grp is vit K dependent…
What factors…

prothrombin

2,7-9,10

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HMWK, PK
11,12 what group

All of these factors are involved in the initial phase of the intrinsic system activation.

contact group

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Group that is not vit K dep, activates instrinsic pathway, includes HMWK, 11,12

contact group

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Intrinsic and common tested with what test

APTT

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factors in intrisic pathway

8,9-11,12

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Factors in extrinsic pathyway

7, 3(TF)

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Extrinsic and common pathway tested with

PT/INR

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factors in common pathway

1,2,5,10

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factor not part of coag pathways and doesn’t affect testing

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what does PT/PTT test for

crosslinked fibrin clot

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fibrinogen

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Prothrombin

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III

Tissue thromboplastin, TF

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calcium

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labile

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VII

stable

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VIII

antihemophiliac A

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antihemophiliac B

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anti hemophiliac C

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Stuart Prower

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XII

Hageman

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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

ISI is used to calculate the INR for the...

Test that monitors wafarin/coumadin

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

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

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