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Back up cards AAB > AABHemOnline2.1.24 > Flashcards

AABHemOnline2.1.24 Flashcards

1
Q

1,5,8-13 what group

A

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

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2
Q

Group not vit k dep, consumed in coagulation, not in serum1,5,8-13

A

fibrinogen group

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3
Q

2,7-9,10 what grop

A

Prothrombin

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4
Q

Which grp is vit K dependent…What factors…

A

prothrombin2,7-9,10

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5
Q

HMWK, PK11,12 what groupAll of these factors are involved in the initial phase of the intrinsic system activation.

A

contact group

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6
Q

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

A

contact group

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7
Q

Intrinsic and common tested with what test

A

APTT

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8
Q

factors in intrisic pathway

A

8,9-11,12

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9
Q

Factors in extrinsic pathyway

A

7, 3(TF)

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10
Q

Extrinsic and common pathway tested with

A

PT/INR

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11
Q

factors in common pathway

A

1,2,5,10

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12
Q

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

A

13

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13
Q

what does PT/PTT test for

A

crosslinked fibrin clot

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14
Q

I

A

fibrinogen

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15
Q

II

A

Prothrombin

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16
Q

III

A

Tissue thromboplastin, TF

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17
Q

IV

A

calcium

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18
Q

V

A

labile

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19
Q

VII

A

stable

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20
Q

VIII

A

antihemophiliac A

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21
Q

IX

A

antihemophiliac B

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22
Q

XI

A

anti hemophiliac C

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23
Q

X

A

Stuart Prower

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24
Q

XII

A

Hageman

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25
Q

XIII

A

fibrin stabilizing

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26
Q

inactive form of plasmin

A

plasminogen

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27
Q

fibrinolysis is breakdown of fibrin by act of

A

plasmin

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28
Q

insoluble fibrin breaks down to

A

D-dimer

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29
Q

soluble fibrin breaks down to

A

FDPs

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30
Q

Thromboplastin (TF, Ca) used in

A

PT

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31
Q

ISI is used to calculate the INR for the…

A

PT

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32
Q

Test that monitors wafarin/coumadin

A

PT

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33
Q

Two methods for PT, PTT, TT

A

optical and electromechanical

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34
Q

PT ref range

A

10-13sec

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35
Q

Increased PT associated with factors…

A

7 extrinsic1,2,5,10 common

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36
Q

Activated partial thromboplastin reagent in aPTT is a

A

phospholipid

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37
Q

Two reagents in aPTT

A

activated partial thromboplastin/phospholipid and CaCL

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38
Q

PTT range

A

30-36sec

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39
Q

Increased aPTT associated with factors…and also this….

A

8,9,11,12 intrinsic1,2,5,10 commoninhibitor

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40
Q

Test that tests amt of time it takes for fibrinogen to convert to fibrin

A

thrombin time

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41
Q

Thrombin reagent used in these two tests

A

TT, fibrinogen

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42
Q

TT ref

A

10-15 secSimilar to PT

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43
Q

increased TT due to

A

A/hypo/dys-fibrinogenemiaHeparinFDPsThrombolytic therapy

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44
Q

Test that tests fibrin clot formation by using Thrombin and plotting clot times w/1:10 std dilution

A

fibrinogen

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45
Q

In testing fibrinogen, concentration is…. …. to clotting timeref range

A

inversely proportional to clotting time, longer time means less fibrinogen200-400mg/dL

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46
Q

Increased fibrinogen in these 3

A

inflammationpregobirth CTRL

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47
Q

decreased fibrinogen in these 3

A

DICliver dysfuctionhypofibrinogemia

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48
Q

Test that differentiates factor def from lupus inhibitor using 1:2 dilution of PT plasmsa to normal pooled plasma running PT/APTT

A

mixing study

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49
Q

If PT/PTT is correct in a mixing study, this indicates a…follow up with a … …

A

factor deffactor assay

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50
Q

If PT/PTT is not corrected with mixing study,indicated an….

A

inhibitor

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51
Q

Factor assay normal range

A

50-100% activity

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52
Q

Test where you do PT,APTT and get std curve from dilutions; times are converted to % activity

A

factor assay

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53
Q

Factory assay should be…

A

linear

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54
Q

Nonlinear in a factor assay indicates

A

inhibitor

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55
Q

Test which uses monoclonal ab to detect fragments

A

D dimer

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56
Q

D dimer ref

A

<=0.50mg/mL

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57
Q

Increased Ddimer in these 4

A

DIC, DVTPulmonary embolismArterial thromboembolism

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58
Q

Test that tests for soluble fibrinogen, FDP with latex agglutination

A

FDP/FSP/fibrin monomer

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59
Q

Most common coagulation disorder, autosomal dominant disease

A

vWD

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60
Q

vWD lacks

A

F8:vWD

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61
Q

vWD:PTT…PFA100/PLT agg…

A

PTT increasedPFA100/PLT agg abnormal

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62
Q

Condition thats recessive sexlinked; hemorragic;F8 def with normal PLT function

A

Hemophilia A

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63
Q

Hemophilia A:PTT..PLT func…

A

PTT increasedPLT func normal

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64
Q

What do vWD and Hemophilia A have in common…How do you diff between vWD and Hemophilia A:

A

Both have F8 def and have increased PTTOnly vWD has abnormal PLT function

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65
Q

Recessive, sexlinked F9 def

A

Hemophilia B

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66
Q

autosomal recessive F11 def

A

Hemophilia C

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67
Q

Def that is part of common pathway where both PT and PTT is increased

A

fibrinogen def

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68
Q

Term when fibrinogen levels are below analytical range

A

A-fibrinogenemia

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69
Q

Term where fibrinogen is <200

A

Hypo-fibrinogenemia

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70
Q

Term where amt of fibrinogen is normal but PT/PTT are increased

A

Dys-fibrinogenemia

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71
Q

Factor def where all tests will be normal because it’s not part of coag pathway

A

F13 def

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72
Q

5M urea solubility test uses urea to dissolve clot, which def is tested using this…positive…

A

F13positive is clot dissolves

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73
Q

Def thats part of intrinsic, theres no history of bleeding and only the PTT is abnormal

A

F12 def

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74
Q

Disorde where theres formation of microthrombi followed by systemic fibrinolysis

A

Disseminated Intravascular coagulation

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75
Q

DIC:PLT ct, fibrinogen..BT, PT, APTT..FSP/Ddimer…

A

PLT ct, fibrinogen: decreased, all used upBT, PT, APTT: decreased, coag factors used upFSP/Ddimer…pos

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76
Q

In Liver disease, all but…are decreased

A

all but F8

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77
Q

In vit K def, what factors are decreased

A

2,7,9,10 vit k dependent

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78
Q

What diff liver from vit k def

A

F8

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79
Q

Lupus anticoagulant seen in…ab against aPTT is…

A

SLEantiphospholipid ab

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80
Q

Lupus anticoag:PTT…rest are…mixing study…

A

PTT is increased but rest are normalmixing study isn’t corrected

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81
Q

Hemotopoetic order

A

HSC, MPP, Common, CFU

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82
Q

Where does hemotopoeisis begin

A

yolk sac

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83
Q

order of hemotopoiesis organs

A

yolk sac, liver, spleen, BM

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84
Q

Medullary/BM/red marrow production of cells in adults in …bones of … and …

A

flat bones of illiac crest and sternum

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85
Q

extramedullary production of cells in adult are… and ….

A

liver and spleen

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86
Q

Pronormoblast is called

A

Proerthyroblast

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87
Q

What cell comes after Pronormoblast/Proerthythroblast

A

Basophlic normoblast/erythroblast

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88
Q

Polychromotaphilic normoblast is also

A

Polychromotaphilic erythroblast

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89
Q

Orthochromatic normoblast also

A

Orthochromatic erthythoblast

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90
Q

Retic is also

A

Polychromatic ertythrocyte

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91
Q

RBC also

A

ertythrocyte

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92
Q

RBC:1.)Pro, 2.)Basophilic, 3.)Polychromatophilic 4.)Orthochromatic…./…..

A

normoblast/erythroblast

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93
Q

Last nucleated red cell, NRBC called these two

A

orthochromatic normoblast, erythroblast

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94
Q

RBC5.)Retic or6.)RBC or

A

5.)polychromatic erythrocyte6.)erythrocyte

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95
Q

Retic called

A

polychromatic erythrocyte

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96
Q

Myeloid cell with red, azurphilic primary granules

A

Promyeloctye

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97
Q

Myeloid with 50% nucleus and specific granules

A

myelocyte

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98
Q

Lymphoid cell that one large prominent nucleoli

A

prolymphocyte

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99
Q

1.)Megakaryoblast2.)Promegakaryocyte3.)Megakaryocyte4.)PLT

A

…

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100
Q

Largest cell in BM, can make 1000 PLTs

A

Megakaryocyte

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101
Q

Diff between mono and promono

A

chromatin is finer/lacy in promono

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102
Q

Hmg:2…2…chains4……ring with…

A

2 alpha, 2 beta4 heme grpsprotoporphyrin ring w/iron

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103
Q

3 embroyonic hmg

A

Gower 1,2,Portland

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104
Q

2 zeta, 2 epsilon

A

gower 1

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105
Q

2 zeta, 2 gamma

A

Portland

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106
Q

2 alpha, 2 epsilon

A

Gower 2

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107
Q

Gower 1: zeta,epsilonGower2:alpha, epsilonPortland:zeta,gamma

A

….

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108
Q

Hmg F chains

A

2 alpha2 gamma

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109
Q

Adult Hmg and %

A

A 97-98A2 2-3F 1

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110
Q

polypedtide chain that is only seen in embryonic

A

epsilon

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111
Q

polypeptide chain thats in both fetal and adult, curve will have sharp incline before birth and be dominant in adult

A

alpha (hmg A,F)

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112
Q

Chain with curve that rises early before birth then decreases after birth

A

gamma

113
Q

chain with curve at minimal rise until right after birth into adult

A

gamma

114
Q

chain with curve thats the lowest and in adults

A

delta

115
Q

Type of EDTA used in hematoloby

A

Di-potassium

116
Q

anticoag in Coagulation, ratio

A

3.2% citrated plasma1:9

117
Q

Cell ct calculation

A

cells x DIL x 10/#sqmm

118
Q

Cause of granular slides, decreased RBC/HCTincreased MCV/MCHC

A

cold agg

119
Q

Hmg concentration uses this method

A

cyan methmg

120
Q

Cyan methmg measures all hmg except

A

Sulf-hmg

121
Q

3 things that falsely affect Hmg

A

lipemiaincreased WBCHmg S/C

122
Q

Average size of cellvolume/cell

A

MCV

123
Q

MCV NV, calculation

A

80-100fLHCT/RBC x 10

124
Q

Microcytic valueMacrocytic…

A

<80fL>100mL

125
Q

Average hmg/cell

A

MCH

126
Q

MCHNV, calculation

A

28-34pgHmg/RBC x 10

127
Q

Hmg concentration/cell

A

MCHC

128
Q

MCHC NV, calculation

A

32-36 g/dL, %Hmg/HCT x 100

129
Q

hypochromic….hyperchromic…

A

<32>36 %

130
Q

degree of anisocytosis

A

RDW

131
Q

RDW NV, aniso

A

12-15>15

132
Q

NRBCs falsey increase…correction calculation…

A

WBCsWBC x 100/nrbc +100

133
Q

Besides NRBCS, what two things increase WBC

A

lrg PLTlyse resistant RBC

134
Q

Fragmented RBCs falsely increase….

A

PLTS

135
Q

increased angle makes a …smeardecreased angle makes a … smear

A

increased angle=thickerdecreased =thinner

136
Q

small drop or big angle could cause a

A

short smear

137
Q

big drop, sml angle could cause a

A

long smear

138
Q

crenated smear due to

A

not dried throughly

139
Q

Wright, Giesma are what kind of stains

A

Romanowsky

140
Q

Two reagents in Romanowsky stain

A

Azure BEosin Y

141
Q

Azure B is….stains….Eosin Y is…stains…

A

Azure B is basic, stains acidEosin Y is acidic, stains basic

142
Q

Buffer to acidic, not enough staining, too much rinsing leads to

A

excessive pink and light staining

143
Q

Buffer too alkaline, prolonged staining, not rinsing well leads to

A

excessive blue and dark staining

144
Q

ESRWM

A

W: 0-20M: 0-15

145
Q

4 causes of increased ESR

A

inflammationincreased plasma proteinsrouleauxRA

146
Q

Retic ct:dye used…disc…NV…

A

NMBMiller disc0.5-1.5%

147
Q

Corrected retic ct calculation

A

Retic ct x PT HCT/45%

148
Q

RPI:uses PT HCT, normal HCT, Retic ct and is over 2 days

A

PT HCT/45% x retic ct/2 days

149
Q

screen for HmgS, uses EDTA, Dithionite, doesn’t differentiate

A

Solubility test

150
Q

Hmg S is insoluble in… …Pos solubility test versus neg

A

Hmg S insoluble in sodium dithionitePos: turbidNeg=transparent

151
Q

Stain used in hmg electrophoresis to visualize bands…meansured with…

A

Ponceau staindensitometer

152
Q

Cellulose 8.6 migration from slow/cathod to fast/anode

A

C, S, F, Acrawl, slow, fast, accelarated

153
Q

Slowest/cathode to fastest/anode in citrate 6.2

A

-FASC+

154
Q

Citrate 6.2 slow/cathode to fast/anode migration

A

F, A, S, C

155
Q

Stain catalyzes oxidation of substance by H2O2-enzyme in primary granules-specific for granulocytes-diff AML from ALL

A

MPOmyeloperoxidase

156
Q

Stains phospholipids, neutral fats, sterol-primary, secondary granules-brown/black-AML vs ALL

A

Sudan Black BSBB

157
Q

Enzyme hydrolyze ester linkages and frees nahthol-diazonium salt causes insoluble pigment-myelogenous cells line-AML vs ALL

A

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.

158
Q

Esterase in mons/macrophages, distinguishes AMML vs AMLmyelomon vs mono

A

alpha naphyl esterase

159
Q

Stains glycogen, magenta-mature granulocytes, monos are posdistinguishing acute lymphocytic leukemia (ALL) and nonlymphocytic leukemia

A

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.

160
Q

Distinguished CML from leukomoid-enzyme is in secondary granules of PMNs-scored

A

Leukocyte ALP

161
Q

LAP score NV…Leukomoid, severe bacterial LAP…vsCML LAP…

A

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).

162
Q

TdT

A

Terminal Deoxynucleotidyl Transferase

163
Q

TdT diff…from…

A

ALL from lymphoma

164
Q

Stain that is nonvital, stains iron in BM

A

Prussian blue

165
Q

Prussian blue increased iron staining in these 3, decreased in 1

A

increased in sidero,hemachromatosis, hemosiderosisdecreased in IDA

166
Q

BM aspirate take from… …in adults

A

illiac crest

167
Q

Light scatter at 90 degree is…scattershows…

A

side, granularity

168
Q

Light scatter at 180 degrees is…scattershows…

A

forwardparticle size

169
Q

Stain uses acid elution, citrate phosphate buffer; eluates all hmg except F…F resist acid elution and are…

A

Kleihauer Betkepink

170
Q

Test that denatures A but F are resistant

A

alkali denature HmgF

171
Q

Denatured hmg inclusions of RBC; supravital stain using NMB

A

Heinz body

172
Q

Test using buffered NaCl with increasing hypotonic slns; amt of hemolysis measures spectrophotometrically

A

Osmotic fragility test

173
Q

osmotic fragility test:NV…increased fragility…seen in…

A

NV 50%fragility <50%spherocytosis

174
Q

Screen for PNH, using low ionic strength sln

A

sugar H2O

175
Q

Test for PCH, antiP

A

Donath Landsteiner

176
Q

Intra or extravascular hmg degrationbiliverdin, bili-albumin, bili diglucurondie, urobilinogen, stercobili

A

extravascular

177
Q

intra or extravascular hmg degrationfree hmg, haptoglobin, methmg, urine hemosideran, heme/Fe, hemopexin

A

Intravascular

178
Q

Hmg in ferrous state, Fe3+

A

oxyhmg

179
Q

hmg oxidized to ferric state Fe2+

A

methmg

180
Q

hmg with carbon monoxide

A

carboxy hmg

181
Q

hmg and CO2

A

Deoxy

182
Q

RBC NV:size, MCV..

A

7-8 microns, 80-100 fL

183
Q

Microcyte…macrocyte…microns, MCV…

A

micro <7, <80fLmacro>8, >100fL

184
Q

Cell with irregular thorn projections/sml bulblike tips; altered lipid content

A

acanthocytes

185
Q

another name for acanthocytes

A

spur

186
Q

cell with bulls eye, increased membrane lipids; decreased hmg, seen in hmg-pathies

A

targets

187
Q

another name for target

A

codocyte

188
Q

crescent, pointed end cell; polymerises into rods of descreased O2 tension; inhibits rouleux

A

sickle cell

189
Q

another name for sickle cell

A

drepanocyte

190
Q

cell with regular projections, reversible/article or liver disease

A

echinocyte

191
Q

another name for echinocyte

A

burr

192
Q

cell pencil/cigar to oval; hereditary, IDA, thall

A

elliptocytes, ovalcytes

193
Q

cell with ecentric vacuole…this cell bursts and becomes…seen in HA, heart vaulve hem

A

blister has ecentric vacuolehelmet burst blister

194
Q

another name for helmet

A

keratocyte

195
Q

cell due to mechanical damage, hemolyze or removed by spleen; fibrin formation caused; TTP,DIC, burns

A

shistocyte

196
Q

cell with MCHC >36, lost biconcave/no CP; increased osmotic fragilityhereditary, ABO incompatibility

A

spherocytes

197
Q

cell with slit like palor, reversibleartifact, increased lipidhereditary, alcoholic, rhnull,lead

A

stomatocyte

198
Q

cell with RBCs inclusions that go thru spleen than elongated, seen in thall/myelofibrosis

A

tear drop

199
Q

another name for tear drop

A

dacrocyte

200
Q

RBC inclusion with blue black evenly distributed coarse to fine granules;seen in lead/thall/hmg-pathies

A

basophilic stippling

201
Q

RBC inclusion red/violet figure 8; remnants of mitotic spindle fibers; severse anema

A

cabbot ring

202
Q

RBc inclusion that’s usually one dark purple spherical granule of DNA; post splenectomy, megablastic, HA

A

Howell jolly bodies

203
Q

RBC inclusion in sml clusters of iron granules seen in wright or PB stain; sideroblastic, thall

A

Pappenheimer bodies

204
Q

RBC inclusion that doesn’t stain with wright, only NMB/supravital;round mass near cell membrane, aggregated denatured hmgG6PD def, drugs, post splenectomy

A

Heinz bodies

205
Q

RBC disorder with amino substituion

A

Hmg-pathies

206
Q

RBC disorder with decreased production of globin chain

A

Thall

207
Q

RBC disorder with decreased RBC etc

A

anemia

208
Q

Hmg-pathy where glutamic acid replaces valine in beta chain, 6th positionhomozygous

A

sickle cell disease

209
Q

In sickle cell disease, what replaces what in the beta chain in the 6th position

A

glutamic acid replaces valine

210
Q

Sickle cell disorder with many sickles, targets, and HJ bodies

A

Sickle cell disease, SS

211
Q

Hmg-pathy heterozygous,glutamic acid replaces valine in beta chain;mostly targets

A

sickle cell trait

212
Q

Hmg-pathy with targets, crytals that look like washington monuments; polychromatophilia

A

Hmg C disease

213
Q

Hmg-pathy with glove like cells, sickle, targets

A

Hmg SC

214
Q

Thallesemia also called Cooleys anemia, micro/hypo; targets, baso stipling,less A, more A2/F

A

Beta Thall major

215
Q

Hmg disorder where >2% Hmg F; hypoxia

A

hereditary persistance HmgF

216
Q

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

A

anemia of chronic

217
Q

anemia with micro/hypobleeding, pregodecreased iron/ferritinincreased transferrin/TIBC

A

IDA

218
Q

anemia thats micro/hypo, increased iron; pappenheimer bodies in wrights, siderocytes in PB, ringed sideroblasts in BM

A

siderblastic anemia

219
Q

Cause of pernicious anemia due to def that affects DNA; macrocytes, hyperseg, megaloblastic

A

folic acid def

220
Q

def that caused pernicious anemia due to lack of IF, can’t absorb B12 for DNA;macro, hyperseg

A

Vit B12 def

221
Q

anemia with pancytopenia, hypocellular BM; drugs/chemo

A

aplastic anemia

222
Q

Membrane defect, enzyme defect, immune and nonimmune are all causes of

A

HA

223
Q

membrane defect where mchc >36, increased osmotic fragility

A

hereditary spherocytosis

224
Q

membrane defect causing hemolysis and occurs at night; testing with sugar H2O, sucrose, HAMs

A

PNHparoxymal nocturnal hmglobinuria

225
Q

Ezyme def that causes HA, cant reduce iron from ferric to ferrous;-seen in antimalarial drugs/fava beans-Heinz bodies

A

G6PD def

226
Q

Cold agglutin disease, paroxymal cold hmg, warm auto are all

A

auto immune HA

227
Q

HDN, hemolytic trans rxn, delay trans rxn are all

A

alloimmune HA

228
Q

HA where RBC/HCT is decreased,MCV/MCH/MCHC all increased

A

cold agg

229
Q

Immune HA where cold auto anti-P, biphasic, complementpos DAT, Donath Landsteiner

A

PCHParoxymal cold hmg

230
Q

HUS, TTP, DIC, plasmodium,babesiabartonella, clostridium can all cause

A

nonimune HA

231
Q

conditon with increased RBC/erythropoeitin; all cells increased;

A

polycythemia vera

232
Q

cell with 3-5 lobes, many secondary granules

A

neutrophil

233
Q

cell with 2-3 lobes, eosin specific granules

A

Eos

234
Q

cell with large dark granules with heparine and histamine

A

Baso

235
Q

Largest cell in blood, horseshoe nucleus/convoluted; lacy chromatin, ground glass vacuoles

A

mono

236
Q

cell nucleus size of RBC, nucleus 90% of cell, condensed chromatin, no nucleoli

A

lymph

237
Q

cell with convoluted light blue, abundant cyto, azurophilic granules

A

large granular lymph

238
Q

cell with ecentric nucleus, coarse chromatin; deep basophillic cyto w/halo of golgi apparatus

A

plasma cell

239
Q

WBC inclusion that are stacks of rough endoplasmic reticulum; light blue, single/multiple;seen in severse bacterial infections

A

Dohle bodies

240
Q

WBC inclusion that are large blue black primary nonspecific granules;bacterial infections and leukomoid rxns

A

toxic granulation

241
Q

WBC inclusions that make clear spots in cyto; seen in bacterial and leukomoid rxn

A

cytoplasmic vacuolozation

242
Q

WBC inclusion seen in AML, red/blue needle in cyto

A

auer rod

243
Q

Two conditions with increased WBC, left shift, Dohle bodies, vacuolization and due to severe bacterial infections

A

reactive neutrophilialeukomoid rxn

244
Q

LAP is… in leukomoid rxn

A

LAP is increased

245
Q

anomoly with hyposegmented segs

A

pelger huet

246
Q

anomoly with azurophilic granules resembling toxic granulation; mucopolyssaccharides

A

Alder-Reily anomaly

247
Q

anomaly with membrane defect of lysosomes, giant abnormal granules;albinism/photophobia

A

Chediak-Higashi anomaly

248
Q

Anomaly with dohle bodies, giant PLTs, but decreased PLTs

A

May Hegglin

249
Q

Gaucher, Tay Sachs, Nieman Pick, Fabrys are all

A

lipid storage diseases w/enzyme def, decreased monos

250
Q

caused by EBV, saliva;10% reactive lymphs, increased WBCs

A

infectious mononucleosis

251
Q

virus spread thru saliva/transfusion;increased WBC, reactive lymphs, negative monospot

A

CMV

252
Q

condition with increased lymphs, negative monospot seen mostly in kids <5yrs of age

A

infectious lymphoctytosis

253
Q

Leukemia affects young, sudden, >20% blasts in BM or blood; can have auer rods;MPO/specific esterase pos

A

AML

254
Q

MPO, SBB, specific esterase posPAS negwhat cell…

A

myeloblast

255
Q

MPO, SBB, specific esterase negPAS poswhat cell

A

lymphoblast

256
Q

AML classifications…M0M1M2

A

M0 minimallyM1 noM2 maturation

257
Q

L1 is what leukemia

A

childhood, TdT

258
Q

L2 is what leukemia

A

adult T cell

259
Q

L3 is what leukemia

A

burkitts,EBV, CALLA, poor prognosis

260
Q

Leukemia in 60yrs older etc, many small mature lymphs/soccer ball, smudge cells

A

CLL

261
Q

Leukemia in 50yrs older, TRAP pos, mononuclear w/hairlike

A

hairy cell

262
Q

leukemia in older males, large bizarre cells with cerebriform nuclei

A

Sezary

263
Q

leukemia in older, myeloid, decreased LAP, many basophilsdry tap, Ph chromosome

A

CML

264
Q

Lymphoma ass w/Reed Sternberg cell,elderly/males

A

Hodgkins lymphoma

265
Q

PLTs:size…volume…live…NV…

A

2-4microns, 10fL7-10days150-450,000

266
Q

Fragmented RBC affect on PLT

A

increase

267
Q

clott/satellism affect on PLT

A

decrease

268
Q

test that test PLT fnc, detects PLT plug, closure timedepends on PLT func, ct, activity

A

PFA 100

269
Q

In PFA 100abnormal collagen/epi indicates

A

aspirin

270
Q

In PFA 100 abnormal collagen/epi/ADP indicates

A

vWD

271
Q

ADAMTS13 def seen in

A

TTP

272
Q

due to ab made to heparin/PF4 complex, PLTs are sensitized and cleared by spleen, decreased PLTs

A

HITheparin induced thrombocytopenia

273
Q

syndrome with giant PLTs, abnormal PLT aggregation with ristocetin

A

Bernard Soulier syndrome

274
Q

Quantitative PLT disorder with decreased giant PLTs and Dohle like bodies

A

May Hegglin

275
Q

PLT aggregation disorder w/ristocetin, glycoprotein 2b/3a defect

A

Glanzmanns thrombasthenia

276
Q

PLT adhesion issue, abnormal ristocetin

A

vWD

277
Q

Two PLT disorders that are abnormal with ristocetin…One that only aggregates with ristocetin…

A

abnormal ristocetin:-vWD, Bernard Soulieronly agg w/ristocetin:Glanzmanns

278
Q

storage pool disease; no granules

A

gray PLT syndrome

279
Q

most common PLT disorder, inhibits thromboxane A2

A

aspirin

Back up cards AAB (19 decks)

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