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Hypercoagulable States: Antiphospholipid Syndrome

The document discusses several hypercoagulable states or inherited conditions that increase the risk of thrombosis. These include antiphospholipid syndrome, factor V Leiden mutation, elevated factor VIII levels, malignant neoplasms, and deficiencies in proteins C, S, antithrombin III. Other conditions mentioned are homocystinuria, prothrombin mutation, plasminogen abnormalities, congenital dysfibrinogenemia. Features like recurrent venous thrombosis, arterial thrombosis, and stillbirth in women are discussed for some of these hypercoagulable states.

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Cora Balaban-Popa
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83 views2 pages

Hypercoagulable States: Antiphospholipid Syndrome

The document discusses several hypercoagulable states or inherited conditions that increase the risk of thrombosis. These include antiphospholipid syndrome, factor V Leiden mutation, elevated factor VIII levels, malignant neoplasms, and deficiencies in proteins C, S, antithrombin III. Other conditions mentioned are homocystinuria, prothrombin mutation, plasminogen abnormalities, congenital dysfibrinogenemia. Features like recurrent venous thrombosis, arterial thrombosis, and stillbirth in women are discussed for some of these hypercoagulable states.

Uploaded by

Cora Balaban-Popa
Copyright
© Attribution Non-Commercial (BY-NC)
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as DOC, PDF, TXT or read online on Scribd
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Hypercoagulable States

Disorder Mechanism There are circulating antibodies that bind plasma proteins with an affinity for phospholipid surfaces, and this can cause thrombosis and in women stillbirth. This syndrome is most often acquired in adulthood, either from an underlying disease or as an idiopathic condition. The two subsets of this syndrome, as defined by laboratory testing, are: lupus anticoagulant (which may or may not be seen with SLE), and anti cardiolipin antibody This is the most common inherited form of hypercoagulability. The mutation, which leads to acti!ated protein " resistance, is present in #$ of "aucasians but is rare in persons of %frican and %sian ancestry. &etero'ygotes ha!e a mild ris( for thrombosis, but the rare homo'ygotes ha!e a mar(ed ris(. % point mutation leads to impaired inacti!ation of factor ) by acti!ated protein ". *ecurrent !enous thrombosis can occur, starting e!en in young persons, and in women stillbirth. This condition is as common as factor ) Leiden mutation. There may be genetic and en!ironmental factors causing it. +ral contracepti!e use increases factor ),,, le!els. The result is deep !enous thrombosis. -eoplastic cells may elaborate a factor, such as a thromboplastin li(e substance, that can increase the ris( for thrombosis. This is one form of paraneoplastic syndrome, with the name Trousseau.s syndrome. There can be !enous (more li(ely) or arterial thrombosis. These conditions are autosomal dominant and lead to recurrent !enous thrombosis, e!en starting in young persons. Thrombosis is often spontaneous, without other precipitating e!ents. They can be detected by laboratory testing for the respecti!e coagulation factor This is an autosomal dominant disorder that can lead to both arterial and !enous thrombosis. Stillbirth may occur in women. Stress is a precipitating e!ent. /ersons with ele!ated plasma homocysteine le!els not only ha!e increased problems with atherosclerosis, but also arterial and !enous thrombosis. Stillbirth may occur in women. The prothrombin 012132% mutation increases the le!el and acti!ity of prothrombin that mildly increases the ris(

Antiphospholipid syndrome

Factor V Leiden mutation

Elevated factor VIII

Malignant neoplasms

rotein !" rotein S" antithrombin III deficiencies Stic#y platelet syndrome

Homocystinemia rothrombin mutation

for arterial and !enous thrombosis. The mutation occurs more often in persons of southern European ancestry.

lasminogen abnormalities !ongenital dysfibrinogenemia

/lasminogen, which has an anticoagulant effect, can be deficient. The features resemble protein " or S deficiency. %lso, tissue plasminogen acti!ator can be deficient. /lasminogen acti!ator inhibitor can be increased. This rare autosomal dominnant disorder may cause either thrombosis or hemorrhage.

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