Laboratory Assessment and Selected Therapeutic Interventions in Hemostasis Flashcards Preview

Heme/Lymph 1 > Laboratory Assessment and Selected Therapeutic Interventions in Hemostasis > Flashcards

Flashcards in Laboratory Assessment and Selected Therapeutic Interventions in Hemostasis Deck (57)
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1

In vivo vs in vitro

In vivo - how it happens in the body...need to understnad for disease
In vitro - how it happens outside the body...important for understanding lab results

2

Platelet count

150-400 thousand/uL
Spontaneous bleeding risk low unless count is <10,000
Thrombotic risk at 1 million

3

Bleeding time

Standardized skin incision
Blot blood flow with filter paper until it comes away clean and measure time til it stops
Preop risk assessment for bleeding...not good

4

PFA-100

Superior to bleeding time
Citrated whole blood aspirated through hole in membrane lined with collagen plus epineprhine or ADP
Activated platelets aggregate
Measure time for platelet plug to occlude hole - closure time

Citrate tube sequesters calcium and only measures primar y

5

Prolonged CT

Thrombocytopenia, vWD, aspirin ingestion, Glanzman, thrombasthenia
not useful for antiplatelet drug monitoring
Good neg predictive value...normal CT means not primary hemostatic dz

6

PLatelet aggregation testing

Platelets concentrated into platelet rich plasma ...various platelet activation facotrs added individually
Activation leads to GP2b/3a mediated aggregation...aggregated clumps fall out of suspension...measurable light transmission increases

Uses light transmission aggregometry

7

Impedence aggregometry

Whole blood...platelet aggregation increases electrical resistance

8

Glanzmann thrombasthenia on LTA

Will show flat line because GP2b/3a receptors don't work and no aggregation

9

Bernard Soulier dz on LTA

Looks normal
Ristocetin must be used to diagnose B-S...binds to vWF and induces conformation change that exposes normally hidden GP1b binding domain, enabling it to agglutinate with platelets

10

Stoarge pool dz on LTA

Heterogenous
Aspirin will flatten the curve like Glanzman

11

Congenital aspirin like defect

Platelets do not respond to arachidonic acid

12

Aggregation vs agglutination

Aggregation - depends on GP2b/3a
Agglutination - depends on GP1b

13

Aspirin affect on platelets

Aspirin irreversibly inhibits platelet COX enzymnes and blocks TXA2 production...inihibits TXA2 mediated platelet activation

Transfers its acetyl group to the COX 1 enzyme

14

GP2B/3a antagonists

Phosphodiesterase inhibitors

GP2B/3a antagonists - block platelet aggregation

Phosphodiesterase inhibitors promote persistance of cyclic AMP and GMP, enhancing platelet inhibitory NO effects

15

THienopyridines

Block platelet activation (clopidogrel and prasugrel)
Permanently bind P2Y12 ADP receptors

16

VerifyNow

Rapid test for aspirin or plavix effect on patients
Employs fibrinogen coated beads whcih aggregate in proportion to GP2B/3A receptors (fewer exposed if more blocked by drug)
Agonist (ADP for plavix and AA for aspirin) activates platelets, exposing GP2B/3S which binds the beads

17

Ristocetin cofactor activity

Test for vWF (%)
Patients native platelets removed and replaced with formlain treated reagent platelets

Formalin treated will agglutinate at rate proportional to concentration

18

ELISA assay for vWF

Uses anti-vWF ABs to quantitate amount

19

Types of vWD and quantitation

1 and 3 - decreased vWF production...protein quantity and activity low
Type 2 - abnormal that may or may not be decreased...activity low but amount may be normal

20

RIPA

Ristocetin induced platelet aggregation - test for type 2B vWD
Should agglutinate at lower concentrations if type 2B because conformation already present
Test for type 2B

If diagnosed, can treat with DDAVP

21

Multimer analysis

Good for vWD
Type 1 and 3 - decrease in all sizes
Type 2 - selective loss of HMW multimers
TTP - increased multimer

22

Clot based test advantages and disadvantages

Well established, available, simple, cheap, familiar
Potentially misleading

23

Clot based tests

Being with platelet poor plasma...excess calcium neutralizes citrate...reagnet phospholipid fills role of removed platelets...clot formation stimulated with an agonist...end point is initial detection of clot

Only for secondary hemostatic dz

24

Endpoint of clot based tests

Fibrinogen to fibrin cleavage (detecting fibrin formation)

25

Where do in vitro and in vivo converge?

Factor 10

26

Common pathway sequecne

10, 2 ,1

27

Extrinsic pathway

Tissue factor, F7, F10, 2, 1

28

Intrinsic pathway

F12 forms with HMWK and PK...F12 cleaves F11...F11 cleaves F9 (needs F8)...cleaes F10...2, 1

29

PTT
PT

Isolated PTT (partial thromboplastin time) prolongation points to extrinsic
Isolated PT (prothrombin time) pointed to F7

30

PTT

Partial thromboplastin time
All elements intrinsic to ciruclation (No TF)
TO start, silica added with Ca and phosphlipids removed

Phospholipids without TF - partial thromboplastin

Commonly used for monitoring unfractionated heparin