Hemodynamic Disorders: Hemostasis Flashcards by ashley f

normal hemostasis includes

platelets
endothelium
plasma clotting factors

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function of platelets

maintenance of vascular integrity
platelet plug formation
platelet phospholipid complex expression (leads to promotion of coagulation cascade)
promotion of endothelial repair

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name 2 platelet inhibitors

cyclooxygenase inhibitors (aspirin)

2. ADP receptor antagonists (ticlopidine and clopidogrel)

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what are other platelet inhibitors

phosphodiesterase inhibitors (dipyridamole)

2. glycoprotein (GP) IIB/IIIa receptor antagoinsts

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mechanism of phophodiesterase inhibitors

increases [ ] of cAMP and cGMP

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function of endothelium

metabolic transfer
barrier functions
synthesis of mediators of interactions between endothelium and blood components
thomboresistance - prevents clotting
mediation of vascular repair

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examples of endothelial thromboresistance

heparin-like molecules
PGI2 and nitric oxide (NO) synthesis
plasminogen activation
ADP degradation
thrombin inactivation
thrombomodulin production
protein S synthesis

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where do heparin-like molecules act at

at interface of endothelial cells and plasma

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function of heparin-like molecules

activate antithrombin III

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activated antithrombin II cleaves

thrombin, factors Xa and IXa

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what is thrombomodulin

endothelial surface protein

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thrombomodulin is a receptor for

thrombin

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thrombomodulin binds thrombin and coverts it to an

activator of protein C

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activated protein C (APC) cleaves factors

VA and VIIIa

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protein S is a cofactor for

activated protein C

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other functions of activated protein C

contributes to significant reduction of mortality in patients with severe sepsis
attenuates various deleterious events induced by lipopolysaccharide (LPS)

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activated protein C has associated —- and — effects

anti-inflammatory

profibrinolytic

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activated protein C inhibits

tumor necrosis factor-alpha (TNF-alpha) production

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events initiated by endothelial disruption

vasoconstriction (neurogenic, endothelin)
platelet adhesion and aggression
release of TxA2
initiation of coagulation
fibrinolysis

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what are the 3 distinct phases of the newest representation

initiation
propagation
termination

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what are initiation

-chemical or mechanical damage to tissue

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function of initiation

exposes tissue factor (TF) to the plasma circulation

- induces TF expression by monocytes, activated endothelium

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Tissue factors interacts with a small amount of

preexistant factor VIIa in the plasma

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interaction of TF and preexistant factor VIIa form

extrinsic tenase (TF/VIIa/IX/X) on a phospholipid surface

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rapid inactivation of the extrinsic tenase by

tissue factor pathway inhibitor (TFPI)

extrinsic tenase generates small amounts of factors

IXa and Xa

Xa cleaves

prothrombin (II) to form small amounts of thrombin (IIa)

initial small amounts of thrombin activates

cofactor proteins factors V and VIII to VA and VIIIa platelets

cofactor activation initiates assembly on

platelet phospholipid surface of intrinsic tenase (VIIIa/IX/X) which leads to Xa activation

function of prothrominase (Va/Xa/II/Ca++)

accelerates thrombin formation (IIa)

thrombin and fibrinogen form

fibrin

function of fibrin

- removal of fibrinopeptide A and B | - cross-linking

termination

formation of thrombin/thrombomodulin complex activates protein C which inactivates Va and VIIIa

how is extrinsic tense inactivated

spontaneous decay of TFPI

inactivation of Xa and thrombin (IIa) by

antithrombin III

prothrombin time (PT) is a measure of

extrinsic pathway of coagulation

Prothrombin Time measures factors

VII, X, V, II and fibrinogen

prothrombin time is a mixture of

thromboplastin (tissue factor) plasma, calcium ion

expect a clot to form in ---s when using PT

12 seconds

partial thromboplastin time is a measure of

intrinsic pathway of coagulation

PTT measures factors

XII, XI, IX, VIII, X, V, II, fibrinogen

PTT is a mixture of

phospholipid platelet substitude (partial thromboplastin), plasma, calcium ions

a clot form in ---s with PTT

25 seconds

name 2 disorder of hemostasis

1. antithrombotic (hemorrhagic) disorder | 2. prothrombotic (hypercoaguable) states

what are the antithrombotic (hemorrhagic) disorders

- classic hemophilia - Christmas disease - von Willebrand's disease - disseminated intravascular coagulation with consumption coagulopathy etc.

what are the prothombotic (hypercoaguable) states

- hereditary thrombophilia - lupus anticoagulant - HIT syndrome (heparin induced thrombocytopenia and thrombosis syndrome) - disseminated intravascular coagulation (DIC)

hereditary thrombophilia is most often present in

adolescents or young women

hereditary thrombophilia presents with

- venous thrombosis | - recurrent thromboembolism

name 2 hereditary thrombophilia

Factor V Leiden Prothrombin 20210A transition Methylene Tetrahydrofolate Reductase Mutation

Factor V Leiden has a mutation in

factor V | causes resistance to activated protein C

what are the 3 Hereditary THrombophilia deficiencies

1. antithrombin III deficiency 2. protein C deficiency 3. protein S deficiency

Genes implicated in hereditary thrombophilia

- factor V Leiden and other factor V variants - prothrombin 20210G-A polymorphism - hyperhomocysteinemia and homocystinuria - antithrombin 3 - protein C - protein S - numerous others

lupus anticoagulant has a prolonged --- test

partial thromboplastin time

in lupus anticoagulant what interfers with PTT test

antiphopholipid antibodies

symptoms of Lupus Anticoagulant

- increased venous and arterial thrombosis | - sometimes associated with autoimmune diseases such as SLE

what is HIT syndrome

heparin-induced thrombocytopenia (and thrombosis)

HIT syndrome is caused by

antibodies to the complex of heparin and platelet factor 4 (PF4)

HIT syndrome is related to what kind of therapy

therapy with high molecular weight heparin (avoided by using low molecular weight heparin)

HIT syndrome is clinically characterized by

heparin induced thrombocytopenia followed by thrombotic complications (cause too much clotting)

disseminated intravascular coagulation (DIC) is caused by

- an obstetric complication caused be: - retained dead fetus - premature separation of placenta (abruptio placentae)

DIC is gram ---- species

negative

DIC can lead to what type of trauma

- leg surgery | - hemolytic transfusion rxns

DIC can cause what type of malignancy

lung, pancrease, other

what is DIC

widespread deposition of fibrin in microvasculature

what factors are involved with DIC

factor VII, V, II and fibrinogen

what is consumption of coagulopathy

- depletion of platelets and coagulation factors | - associated with DIC

DIC has prolongation of

- prothrombin time (V,II, fibrinogen) - PTT (VIII, V, II, fibrinogen) - thrombin time (fibrinogen)

DIC has presence of

fibrin-fibrinogen degradation (split) products (FDP)