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Notes in
L21 + L22 - Hemostasis
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Published
11/02/2024
Primary hemostasis is the {{c1::the formation of platelet plugs}} in response to {{c1::vascular injury/endothelial damage}}
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11/02/2024
Thrombocytopenia is defined as a platelet count below {{c1::100,000}} whereas thrombocytosis is defined as a platelet level over {{c1::400,000}}
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In addition to their involvement in primary hemostasis, platelets also:1. {{c1::provide a phospholipid surface and calcium ions for the coagulation ca…
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11/02/2024
In the healthy state, endothelial cells do not react with platelets (or any other blood components) due to:1. {{c1::repelling negative charges of both…
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Endothelial damage is most commonly caused by:{{c1::Lacerations}}{{c1::Hyper}}tensionHigh {{c1::cholesterol}}{{c1::Smoking::lifestyle choice}}
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11/02/2024
Following endothelial cell injury, {{c1::collagen}} of the subendothelium and {{c1::von Willebrand factor (vWf) from weibel palade bodies}} are expose…
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11/02/2024
Thromboxane A2 is produced via the {{c1::cyclooxygenase}} pathway of arachidonic eicasanoid synthesis
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Platelets that cannot produce {{c1::thromboxane A2}} cannot induce platelet aggregation or participate in the platelet plug
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When a platelet is activated, a conformational change is induced in the glycoprotein integrin receptor {{c1::Gp IIB-IIIA}} which allows it to then bin…
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Fibrinogen functions primarily in platelet aggregation by {{c1::linking platelets to one antoher via Gp-IIb-IIIa receptors}}
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Thrombin is a product of {{c1::secondary}} hemostasis that induces further platelet aggregation and the release of TXA2, serotonin, and ADP
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During secondary hemostasis, fibrinogen is cleaved to {{c1::fibrin}} which functions to {{c1::stabilize the primary hemostatic plug (form a secondary,…
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11/02/2024
Bernard-soulier syndrome.Inheritance pattern: {{c1::autosomal recessive}}Deficiency: {{c1::Gp-Ib-IX}}Pathophysiology: {{c1::impairs the ability of pla…
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11/02/2024
Glanzmann thrombasthenia.Inheritance pattern: {{c1::autosomal recessive}}Deficiency: {{c1::Gp IIb-IIIa}}Pathophysiology: {{c1::defective platelet…
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vWF is a carrier for {{c1::Factor VIII}}
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von Willebrand disease type I is caused by {{c1::an underproduction of vWF}}. It is treated by {{c1::desmopressin}} which functions to {{c1::stimulate…
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von Willebrand disease type II is caused by {{c1::a normal quantity of defective vWF}}. It is treated with {{c1::desmopressin}} which functions to {{c…
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11/02/2024
vWF is encoded on chromosome {{c1::12}}, therefore, von Willebrand diseases are inherited in an {{c1::autosomal}} fashion
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von Willebrand disease type III is caused by {{c1::a complete absence of vWF}}. It is treated with {{c1::vWF and Factor VIII infusions}}
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Which form of von Willebrand disease is the most severe?{{c1::Type III}}
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Which form of von Willebrand disease is the most common?{{c1::Type I}}
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What are the common clinical features of von Willebrand diseases?{{c1::frequent nosebleeds, excessive hemorrhage following trauma/surgery, menorrhagia…
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What is the most common bleeding disorder worldwide?{{c1::von Willebrand disease}}
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11/02/2024
Excess primary hemostastis may be treated with {{c2::aspirin}} which is a(n) {{c1::irreversible}} inhibitor of {{c1::cyclooxygenase}}, preventing the …
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11/02/2024
Platelet aggregation can also be inhibited by corticosteroids through their inhibition of {{c1::the arachidonic acid pathway}}
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11/02/2024
Platelet aggregation can by inhibited by {{c2::Gp IIb-IIIa}} inhibitors like {{c1::abciximab}}, {{c1::eptifibatide}}, and {{c1::tirofiban}}.…
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11/02/2024
Platelet aggregation may also be inhibited by {{c2::ADP (P2Y12)}} receptor inhibitors such as {{c1::clopidogrel (Plavix) or ticlopidine}}
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11/02/2024
Secondary hemostasis primarily involves the formation of {{c1::fibrin (factor Ia)}} to {{c1::stabilize the platelet plug}}
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The intrinsic pathway of coagulation relies on components {{c1::in the plasma::location}} to form a stable clot
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The extrinsic pathway of coagulation relies on {{c1::Tissue factor (factor III)}} to initiate the coagulation cascade
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The {{c1::extrinsic}} pathway of coagulation initiates fibrin/stable clot formation while the {{c1::instrinsic}} pathway continues and amplifies the p…
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The proteases involved in secondary hemostasis are primarily found in the {{c1::plasma, in a zymogenic state}}
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Following vascular injury, the first step in the extrinsic pathway is {{c1::the binding of tissue factor (Factor III) with Factor VII}}
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Association of Factor VII with tissue factor forms an inactive complex that is activated by {{c1::Factor VIIa, IXa, Xa, or thrombin}} requiring {{c1::…
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Factor X is activated by {{c1::Factor VIIa (complexed with the tissue factor)::extrinsic pathway}} or {{c1::Factor IXa - Factor VIIIa::intrinsic pathw…
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Factor Xa activates {{c1::prothrombin (factor II)}} to {{c1::thrombin (Factor IIa)}} requiring {{c1::calcium, phospholipids, vitamin K, and Factor Va}…
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11/02/2024
Thrombin (Factor {{c1::IIa}}) activates Factors {{c1::I, II, V, VII, VIII, XI, and XIIII}}
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11/02/2024
Factor XIIIa functions as a transglutaminase to {{c1::crosslink fibrin}}
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Proteins {{c2::C and S}} are activated by {{c1::thrombin}}, and function to destroy Factors {{c1::Va and VIIIa}}
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Factor IX is activated by either Factor {{c1::XIa}} or {{c1::VIIIa}}
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Hemophilias.A is caused by a deficiency in {{c1::Factor VIII}}B is caused by a deficiency in {{c1::Factor IX}}
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11/02/2024
Hemophilia A is an {{c1::X-linked recessive::inheritance pattern}} disorder
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Hemophilia B is an {{c1::X-linked recessive::inheritance pattern}} disorder
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Hemophilias are often characterized by frequent bleeding into {{c1::joints}} and {{c1::muscles}}
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11/02/2024
Patients with hemophilias have {{c1::normal}} bleeding times
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{{c2::Tissue factor pathway inhibitor (TFPI)}} is a protease inhibitor of Factors {{c1::VIIa and Xa}}
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TFPI (tissue factor pathway inhibitor) is produced by {{c1::endothelial cells}}
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11/02/2024
TFPI (tissue factor pathway inhibitor) exerts its function by binding to Factor {{c1::Xa}} and ultimately forming a complex with Factor {{c1::VIIa}} t…
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11/02/2024
Protein Ca deficiency is a risk factor for {{c1::thrombosis}}
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11/02/2024
Protein S deficiency is a risk factor for {{c1::thrombosis}} and is often associated with {{c1::TFPI (tissue factor pathway inhibitor)}} deficiencies
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11/02/2024
Factor V leiden patients have a mutant form of Factor V that causes an increased risk for {{c1::thrombosis}} due to {{c1::its inability to be cleaved …
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Fibrinolysis is acheived through the activation of {{c1::plasminogen}} to {{c1::plasmin}} by {{c1::tissue plasmin activator (tPA)::endogenous}}, produ…
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Fibrin cleavage produces {{c1::D-dimer}}
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Plasmin is endogenously inhibited by the enzyme {{c1::α2-antiplasmin}}
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11/02/2024
tPA can be inhibited by the enzymes {{c1::PAI-1 and 2 (plasminogen activator inhibitors 1/2)}}
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11/02/2024
The most common prothrombin mutation is caused by a mutation in the {{c1::3' UTR}} which results in {{c1::elevations}} in serum prothrombin leading to…
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11/02/2024
{{c1::Non-O}} type blood exhibits a greater risk for thrombophilia due to increases in {{c1::vWF}}
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11/02/2024
Heparin can be neutralized with {{c1::protamine}}
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11/02/2024
Warfarin is a {{c1::vitamin K}} antagonist that prevents the {{c1::γ-glutamly carboxylation}} of nascent Factors {{c1::II, VII, IX, and X}} and p…
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11/02/2024
Warfarin toxicity is reveresed by IV {{c1::vitamin K}}
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11/02/2024
{{c2::Xarelto (rivaroxaban)}} and {{c2::eliquis (apixaban)}} are pharmacologic {{c1::Factor Xa}} inhibitors
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11/02/2024
Gamma carboxylation of the coagulation factors allows them to {{c1::bind calcium}}
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11/02/2024
tPA can only be used to treat {{c1::prexisting}} clots
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Warfarin is slow acting due to the fact that it {{c1::does not alter pre-existing coagulation factors}}
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What factors are involved in the intrinsic pathway?{{c1::Factors VIII, IX, XI, XII}}
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What factors are involved in the extrinsic pathway?{{c1::Factors III (TF) and VII}}
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The therapeutic efficacy of warfarin can be undermined primarily through {{c1::diet and vitamin K supplementation}}
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11/02/2024
platelets, which are also called {{c1::thrombocytes}}, are derived from {{c1::megakaryocytes}} and function to {{c1::maintain vascular integrity}} thr…
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the normal concentration of platelets is {{c1::150,000 - 300,000}} / μl of blood
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{{c1::thrombus}} is a pathological clot of endothelium
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{{c1::thrombosis}} is an abnormal internal clot that is not beneficial
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von Willebrand factor (vWf) is important in {{c1::platelet adhesion to the injured endothelial region}}
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11/02/2024
the adherence of plateletes to glycoprotein (Gp) receptors results in {{c1::platelet activation}}
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11/02/2024
activated platelets release {{c1::ADP, which binds the platelet surface}} and {{c1::Thromboxane A2 (TXA2)}}
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11/02/2024
activated platelets {{c1::recuit other platelets and aggregate}}
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11/02/2024
platelet activation induces a conformational change in {{c1::Gp IIb-IIIa}} that allows platelets to bind to {{c1::fibronogen}} with high affinity
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11/02/2024
Gp IIb-IIIa is a member of the {{c1::integrin}} family
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11/02/2024
{{c1::fibrinogen}} and {{c1::thrombin}} are potent inducers of platelet aggregation
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11/02/2024
Gp IIb-IIIa binds fibrinogen that leads to the formation of {{c1::larger platelet aggegates}}
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11/02/2024
{{c1::TXA2}} is required for formation of platelet aggregates and a platelet plug
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11/02/2024
{{c1::platelet receptor inhibitors}} bind to glycoprotein (Gp) receptors on platelets and prevent their binding to the normal ligand
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11/02/2024
aspirin is an {{c1::antiplatelet agent}}, not an {{c1::anticoagulant}}, and doesn't "thin" the blood
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11/02/2024
thrombin cleaves {{c1::"tufts"}} off of fibrinogen to produce fibrin and allow for {{c1::noncovalent association }}
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11/02/2024
antithrombin is a protease inhibitor that {{c1::irreversibly}} inhibits {{c1::thrombin}} ,{{c1::Factor Xa}}, and {{c1::Factor IXa}}
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11/02/2024
antithrombin defieicney is a risk factor for {{c1::thrombosis}}
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11/02/2024
in the presence of {{c1::heparin}} and {{c1::heparan sulfate}}, antithrombin's inhibition of coagulation is {{c1::>1000x}} faster
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11/02/2024
a large fragment of at least {{c1::16}} heparin residues is necessary for increasing the rate of reaction b/w {{c1::antithrombin}} and {{c1::thrombin …
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11/02/2024
low molecular weight (MW) heparin is used to inhibit {{c1::Factor Xa}} but can not inhibit {{c1::thrombin}}
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11/02/2024
people with antithrombin deficiency will not respond to {{c1::heparin anticoagulation therapy}} because {{c1::heparin only works if there's antithromb…
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11/02/2024
Protein C/S pathway:1. {{c1::thrombin}} binds to {{c1::thrombodulin (TM)}} on the endothelium2. {{c1::Protein C}} binds to this altered thrombin and i…
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11/02/2024
{{c1::thrombophilia}} is an increased risk of forming pathological clots
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11/02/2024
A change ({{c1::Arg}} → {{c1::Gln}}) in Factor V leads to the Leiden mutation, which results in Factor V Leiden {{c1::remaining active longer}} than n…
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11/02/2024
what are the inherited risks for thrombosis (6)?{{c1::antithrombin deficiencyprotein C or protein S deficienciesFactor V Leidenprothrombin mutaitonnon…
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11/02/2024
fibrinolysis refers to the breakdown of the {{c1::fibrin clot}}
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11/02/2024
{{c1::bleeding}} is the principal complication of heparin therarpy
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11/02/2024
Heparin-induced thrombocytopenia (an immune reaction) induces {{c1::clotting}}, not bleeding
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11/02/2024
{{c1::bleeding}} is the main complication of warfarin therapy and can be treated by {{c1::vitamin K}}
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11/02/2024
the 3 clot-dissolving drugs are {{c1::t-PAu-PAstreptokinae}}which break down {{c1::existing clots}} and do NOT {{c1::inhibit formation of new clo…
Status
Last Update
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