Page 582 - Clinical Hematology_ Theory _ Procedures ( PDFDrive )

566 PART 7 ■ Principles and Disorders of Hemostasis and Thrombosis

Risk actors or eve o ing hy ercoagu abi ity inc u e
Primary and Secondary
TABLE 28.11
Hypercoagulable States ■ History o thro bosis

■ Inherite an acquire thro bo hi ia
Primary ■ Materna age ess than 35 years o age

Hypercoagulable Secondary ■ Certain e ica con itions an /or co ications o reg-

States Hypercoagulable States nancy an chi birth

Antithrombin II de ciency Cancer
General Features
Protein C de ciency Pregnancy

Protein S de ciency Oral contraceptive use Vascular Dam age and Blood Flow

Fibrinolytic abnormalities Nephrotic syndrome Vascu ar en othe ia a age ex oses circu ating b oo to sub-

en othe ia structures that initiate thro bosis. Constriction
Hypoplasminogenemia Myeloproliferative disorders
o b oo vesse s a itiona y creates stasis. T ro bosis can
Dysplasminogenemia Hyperlipidemias begin in areas o ow b oo f ow or in situations in which the

Tissue plasminogen activa- Diabetes mellitus viscosity o b oo is increase . In atients with a high risk o

tor release de ciency thro bosis, the concentration o brinogen is o en e evate .

Paroxysmal nocturnal High concentrations o brinogen ay in uce aggregation

hemoglobinuria o circu ating erythrocytes, which ro uces increase b oo
viscosity. T is ay encourage thro bosis by ecreasing the
Increased levels of Postoperative states

plasminogen b oo f ow at critica sites with the accu u ation o activate
c otting actors.
Activator inhibitor Vasculitis

Dys brinogenemia APS Platelets

Homocystinuria Increased levels of factor VII Stasis akes it easier or ate ets to be etache ro f ow-

and brinogen ing b oo . An increase in the nu ber o circu ating ate ets

Heparin cofactor II Anticancer drugs ay create a ten ency towar thro bosis. P ate ets accu u-

de ciency ate at the site o vascu ar a age, where they can urnish
hos ho i i or the intrinsic athway an a so ro ote
Increased levels of Heparin thrombocytopenia

histidine-rich GP thro bin or ation by a sorbing activate actor X ro
as a to their sur aces. High ate et counts a itiona y
Obesity oster thro bosis.

Another ossibi ity is that a thro botic ten ency ay be
three ajor hysio ogic anticoagu ant syste s o rotein C, cause by qua itative a terations in ate ets. T ese a terations

antithro bin an tissue actor inhibitor. ay be cause by intrinsic ate et e ects or by changes in

the surroun ing as a. Qua itative abnor a ities ay
Pregnancy-Associated Thrombosis resu t in s ontaneous aggregation, enhance sensitivity to

aggregating agents, or increase a hesiveness.
Nor a regnancy beginning at the ti e o conce tion is

associate with increase concentrations o coagu ation ac-

tors VII, VIII, an X an vWF. In a ition, a signi cant change Blood Clotting Factors

in brinogen is note . Free rotein S, the active, unboun Congenita an acquire hy ercoagu ab e states arise when

or , is ecrease uring regnancy. P as inogen activator there is an i ba ance between the anticoagu ant an ro-

inhibitor (PAI)-1 eve s are increase ve o . P as inogen thro botic activities o as a in which the rothro botic

activator inhibitor (PAI-2) ro uce by the acenta increases activities re o inate.

signi cant y uring the thir tri ester. T ro bin generation A ten ency towar thro bo hi ia (abnor a thro bo-

arkers, or exa e, rothro bin F1+2, an thro bin- sis) ay be cause by qua itative a terations in b oo c ot-

antithro bin co exes are a so increase . It ay take u to ting actors or an increase titer o activate c otting actors

8 weeks a er e ivery ( ost artu ) or the eve s o the cite that can create a ten ency towar thro bosis. T ese actors

constituents to return to the re erence range. can contribute to thro bosis in that activate actors ight

Pregnant wo en have an increase risk o thro boe bo- reach critica eve s in the circu ating b oo .

is because o hy ercoagu abi ity. T e con ition o hy er-

coagu abi ity in regnancy is ost ike y evo ve to rotect Factor V (Leiden)

wo en against the b ee ing cha enges o chi birth or is- T e actor V gene is an autoso a , co o inant y inherite

carriage. Pregnant wo en are at a our- to ve o increase gene. Factor V R506Q (Lei en) utation is the ost co -

risk o thro boe bo is uring regnancy an the ost ar- on un er ying genetic cause o thro bo hi ia (e.g., venous

tu erio co are to non regnant wo en. Eighty ercent thro bosis).
o the thro boe bo ic events in regnancy are venous with Factor V (Leiden) utation resu ts ro a G-A oint

506
an inci ence o 0.49 to 1.72 er 1,000 regnancies. utation that resu ts in an Arg -G y substitution in the