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32 Cards in this Set

  • Front
  • Back

hemostasis definition

tightly regulated processes that maintainblood in a fluid, clot-free state in normal vessels while inducing the rapidformation of a localized hemostatic plug at the site of vascular injury.

the pathologic form of hemostasis

thrombosis; it involves blood clot (thrombus) formation in an uninjuried vessels or thrombotic occlusion of a vessel after relatively minor injury.

both hemostasis and thrombosis involve what 3 components

Vascular wall, platelets and the coagulation cascade.

the balance between what and what determines whether thrombus formation, propagation, or dissolution occurs

anti - and prothrombotic activities

at baseline, endothelial cells exhibit what 3 properties

antiplatelet, anticoagulant, and fibrinolytic properties

on the other hand after injury they are capable of

exhibiting numerous procoagulant activites; They also can be activated by infectious agents, hemodynamic factors and cytokines

antithrombotic properties of endothelial cells

Inhibiting platelet adherence; Preventing coagulation factor activation; Lysing blood clot that may form.

prothrombotic properties of endothelial cells

Endothelial cells can be stimulated by direct injury or various cytokines that are produced during inflammation; Such stimulation results in expression of procoagulant protiens (e.g., tissue factor and vWF (von wilibrant factor))that contribute to local thrombus formation; Also, loss of endothelial integrity exposes underlying vWF and basement membrane collagen, both substrates for platelet aggregation and thrombus formation.

after vascular injury what happens

Vasoconstriction; Subendothelial extracellular matrix; Tissue factor (Factor III/thromboplastin); Thrombin; Polymerized fibrin and platelet aggregates

platelets: what is their role, what do they express

They play a critical role in normal hemostasis.; When circulating and nonactivated they are smooth disks; They express several glycoprotein receptors and contain two types of granules



after vascular injury platelets undergo what 3 reactions

Adhesion and shape change; Secretion (release reaction); Aggregation

platelet aggregation

Endothelial injury exposes the underlying basement membrane ECM; platelets adhere to the ECM and become activated by binding to vWF through GpIb (KNOW THIS ONE) platelet receptors; Upon activation, platelets secrete granule products that include calcium (activates coagulation proteins) and ADP (mediates further platelet aggregation and degranulation); Activated platelets also synthesize TXA2 (thromboxane A2) (increases platelet activation and causes vasoconstriction); Activated platelets provide phospholipid complexes which are an important surface for coagulation-protein activation; Released ADP stimulates formation of aprimary hemostatic plug by activating platelet GPIIb-IIIa (KNOW THIS ONE) receptors that BIND FIBRINOGEN AND CAUSE FIBRINOGEN cross-linking; The formation of definitive secondary hemostatic plug requires the activation of thrombin to cleave fibrinogen and form polymerized fibrin via coagulation cascade

coagulation cascade

The coagulation cascade constitutes the third component of the hemostatic process and is the a major contributor to thrombosis; Coagulation occurs through the sequential enzymatic conversion of a cascade of circulating and locally synthesized proteins; Tissue factor elaborated at sites of injury is the most important initiator of coagulation cascade; At the final stage of coagulation, thrombin converts fibrinogen into insoluble fibrin, which helps to form the definitive hemostatic plug

coagulation is normally restricted to the sites of vascular injury by:

Limiting enzymatic activation to phospholipid complexes provided by activated platelets; Natural anticoagulants elaborated at sites of endothelial injury or during activation of the coagulation cascade.

contact system: includes what, made where, does what, deficiencies, recommendation in some pts

Includes factor XII (Hageman factor), prekallikrein (PK; Fletcher factor), high molecular weight kininogen(Fitzgerald factor); some authors include factor XI; Made in the liver (ECXCEPT FACTOR VIII AND vWF); Decreased activity is associated withliver disease, hepatic immaturity in newborns, antiphospholipid syndrome, Asian descent (for factorXII); Homozygous deficiencies are rare,autosomal recessive; cause prolong PTT but no bleeding disorders and no definite association with hypercoagulability; Recommended to not measure their activity in routine evaluation of patients with arterial or venous thromboembolism oracute coronary syndromes

intrinsic pathway: involves what

Involves factors VIII, IX, XI, XII (Hageman factor), prekallikrein, high molecular weight kininogen; Merges with extrinsic pathway into common pathway; Activated when factor XII binds to negatively charged “foreign” surface exposed to blood; Then sequentially activates factors XI,IX, X, then factor II (prothrombin to thrombin), which converts fibrinogen to fibrin (see common pathway); REMEMBER THIS BY REMEMBERING THE LAST LETTER LEADING TO THE NEXT ONE= twelevE --> EleveN --> NinE -- > EighT --> Ten

extrinsic pathway: involves what

Involves tissue factor (TF), originally considered “extrinsic” to blood since it is present on cell surfaces not normally in contact with (i.e. extrinsic to the circulatory system); The primary mechanism of the coagulationpathway in vivo is tissue factor binding to activatedfactor VII (factor VIIa) (KNOW THIS ONE); TF-Factor VIIa complex activates factors X; Activated factor X with activated factor V, anionicphospholipids (from activated platelets) and calcium as cofactors; convert prothrombin to thrombin

common pathway: involves what

Involves factor I (fibrinogen), factors II (prothrombin), V, X (KNOW THESE); Thrombinconverts soluble fibrinogen to insoluble fibrin; FactorXIII (KNOW THIS) cross links fibrin to increase stability of fibrin clot

causes of excessive bleeding

Increased fragility of vessels; Platelet deficiency or dysfunction; Derangement of coagulation; Combination of the above

bleeding disorders in general: what to look at in clinical history

(A) Single site (structural lesion) vs. multiple sites (coagulopathy); (B) For coagulopathies - hereditary (family history of bleeding or bleeding since childhood) or acquired (no previous bleeding history); (C) Time from “hemostasis challenge” to bleeding symptoms - immediate suggests platelet disorder (inability to form normal platelet plug); late suggests coagulopathy (breakthrough bleeding occurs after platelet plug due to impaired fibrin formation); (D) Physical exam: petechiae (platelet disorders) vs. hematomaor hemarthrosis (coagulation defects) vs. mucous membrane bleeding or bruising (nonspecific)

Bleeding disorders are often classified as defects of

primary hemostasis (platelets, vessels) or of secondary hemostasis (coagulation cascade and its regulation)

tests used to evaluate hemostasis

Bleeding time; Platelet function tests; Platelet counts; Prothrombintime (aka PT); Partial thromboplastin time (PTT); Factor assays; Fibrinogen; Fibrin split products; Circulating anticoagulants

prothrombin time assay used for what

The PT assay screens for the activity of the proteins in the extrinsic pathway (all the way through the common pathway); PT is used to monitor the efficacy of coumadin anticogulantion therapy

PT is prolonged in:

Factor VII deficiency; Common pathway defect (I,II, V&X); Warfarin use or overdose; Heparin overdose or contamination

international normalized ratio (INR): used for what, range, defined as

Used to standardize prothrombintime (PT) results for patients taking warfarin (coumadin); Therapeutic goal is usually a value of 2 to 3; Intended to make comparisons similarbetween different labs by compensating for variable thromboplastins used in PT test; Defined as patient PT divided by mean normal PT, with the result raised to the power (exponent) of the ISI (don't need to know equation)

APTT: screens for what, is useful for what, is prolonged in what

The PTT assay screens for the activity of proteins in the intrinsic pathway; It is useful to monitor the efficacy of heparin therapy for acute thrombosis or embolism It is prolonged in= Common pathway defect, Heparin use, Factor deficiency, DIC

TT: prolonged in what

tests only for fibrogen (factor I); Hypofibrinoginemia; Dysfibrinoginemia; Heparin use or contamination; DIC

test battery: APTT abnormal, PT abnormal, TT normal, possible causes?

Vitamin K deficiency (Factors II, VII, IX & X deficiency); Liver diseases; Inhibitor effect; answer= Factor deficiency in common pathway II, V, X

test battery: APTT abnormal, PT normal, causes?

Factor deficiency in intrinsic pathway; Antiphospholipid antibody; Specific factor inhibitor= FVIII inhibitor; ANSWER= both extrinsic and common are normal because of normal PT so the problem must be in the intrinsic pathway

test battery: APTT normal, PT abnormal, causes?

Factor deficiency in the extrinsic pathway; Specific factor inhibitor; ANSWER= APTT normal so normal intrinsic factor, PT abnormal so problem in the extrinsic pathway

test battery: APTT abnormal, PT abnormal, TT abnormal, causes?

Factor deficiency; Severe liver diseases; DIC; Potent inhibitor; Fibrinogen abnormality