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Gen Path Exam 2 > Overview of Hemostasis and Coagulation > Flashcards

Overview of Hemostasis and Coagulation Flashcards

1
Q

What is hemostasis?

A

-ability to maintain blood in a fluid state and prevent loss from sites of vascular damage

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2
Q

What are the 3 major components of the hemostatic system?

A

-vascular wall, platelets and coagulation proteins

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3
Q

What are the three A’s of platelet response?

A
  • adhesion
  • activation
  • aggregation
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4
Q

What happens during the adhesion stage of platelet response to vascular injury?

A
  • platelets adhere to to damaged endothelial site

- this involves the activation of a surface membrane receptor, an adhesive protein and an appropriate surface

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5
Q

What does von Willebrand factor do?

A
  • mediates adherence of platelets to the subendothelial collagen
  • glycoprotein Ib binds to vWF
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6
Q

What happens during the activation stage of platelet response to vascular injury?

A
  • additional platelets are recruited
  • second messenger molecules released after binding to vWF that lead to shape change from disc to sphere, secretion of ADP, activation of glycoprotein IIB and IIIa receptor
  • contraction of platelet mediated though actin fibers
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7
Q

What happens during the aggregation stage of platelet response to vascular injury?

A
  • Platelets interacting with other platelet
  • release of cytoplasmic ADP into local milieu causes activation of adjacent platelets
  • platelet-platelet binding mediated through fibrinogen and gp IIb/IIIa receptor
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8
Q

What conversion adds stability to the clot after fibrin cross-linking by Factor XIII?

A

-Thrombin converts fibrinogen to fibrin

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9
Q

What is the intrinsic pathway of clot formation?

A
  • activation of Factor XII by kallikrein
  • activation of Factor XI by Factor XIIa
  • Factor XIa activates Factor IX
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10
Q

What is the extrinsic pathway of clot formation?

A

-activation of Factor VII by tissue factor

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11
Q

What is the common pathway of clot formation?

A
  • activation of X to Xa
  • conversion of prothrombin II to thrombin
  • conversion of fibrinogen I to fibrin monomers
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12
Q

A fibrin clot is formed by fibrin monomers generated by what polymerize and what stabilizes these strands?

A
  • thrombin generates fibrin monomers for polymerization

- monomers are made more stable by covalent cross-linking by factor XIII

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13
Q

Secondary hemostasis is defined by regulation of coagulation. What are antithrombins?

A

-inhibition of thrombin and Factors IXa-XIIa of coagulation cascade through formation of inactive enzyme-inhibitor complex

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14
Q

What is the best known antithrombin?

A
  • antithrombin III
  • in presence of heparin, becomes activated so that it can form a complex with thrombin
  • destroys ability of thrombin to participate in generation of fibrin monomers
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15
Q

What is the function of the protein C system?

A
  • regulation of major cofactors of the coagulation cascade Factors Va and VIIIa
  • Activated protein C is major effector enzyme; protein S is major cofactor
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16
Q

Protein C or Protein S deficiencies result in what issues?

A

-hypercoagulable states

17
Q

How does Factor V Leiden mutation promote coagulation?

A

-resistance to enzyme inactivation by the Protein C/S complex

18
Q

What is fibrinolysis?

A
  • limits generation of fibrin clot
  • in presence of fibrin, tissue plasminogen activator can bind to plasminogen and convert to plasmin
  • plasmin breaks down previously cross-linked fibrin monomers into fibrin degredation products
19
Q

Uncontrolled activation of plasmin can result in what complications?

A
  • bleeding complications due to fibrinolysis

- and fibrinogenolysis

20
Q

What is prothrombin time?

A
  • measurement of time needed for plasma to form a clot in the presence of added tissue thromboplastin and calcium ions
  • Prolonged PT can result from decreases or abnormalities in in Factors II, V, VII, X and fibrinogen
  • routinely used to measure degree of anticoagulation in patients receiving oral anticoagulants
21
Q

What is the international normalized ratio?

A
  • ratio of patient PT time/control PT time

- allows to compare between lab and anticoagulant patients

22
Q

What is partial thromboplastin time?

A
  • PTT
  • measurement of time needed for plasma to form a clot in the presence of added ground glass or kaolin, cephalin and calcium ions
  • used to measure degree of anticoagulation in patients receiving heparin
23
Q

What is thrombocytopenia?

A

-decrease in platelet number

24
Q

What is thrombocytosis?

A

-increase in platelet number

25
Q

What is the normal range for bleeding time?

A
  • 2-8 min

- prolonged when there are abnormalities of platelet number or function

26
Q

What is the significance of mixing study results?

A
  • If clotting time is corrected then there is a deficiency of some factor
  • if clotting time is not corrected, then a factor-specific or lupus anticoagulant type of inhibitor might be present
27
Q

What are the characteristics of disorders of primary hemostasis?

A
  • mucocutaneous bleeding/bleeding associated with trauma

- lab manifestations include a prolonged bleeding time and/or thrombopenia

28
Q

What are the characteristics of disorders of secondary hemostasis?

A
  • soft tissue bleeding
  • bleeding associated with trauma
  • lab manifestations: prolonged PT/PTT and/or thrombin time
29
Q

What are the characteristics of disorders of the regulatory system?

A
  • soft tissue bleeding/bleeding on trauma

- lab manifestations: normal

30
Q

What is Factor VIII Complex?

A
  • set up for vWF disease and hemophilia
  • this is composed of vWF and factor VIII procoagulant
  • Factor VIII is released from vWF when clot is formed
  • Factor VIII participates in the generation of Factor X
31
Q

What are the characteristics of von Willebrand disease?

A
  • AD disorder
  • decreased production of vWF
  • Most common inherited, 1% of pop affected
  • clinical signs: mucocutaneous bleeding
  • leads to decreased production of Factor VIII
  • lab findings: prolonged bleeding, prolonged PTT and decreased vWF & VIII
  • desmopressin for mild cases
32
Q

What are the characteristics of Hemophilia A?

A
  • X recessive
  • decreased production of VIII
  • most common hereditary cause for serious bleeding- hemarthrosis, intramuscular hematomas, intracranial hemorrhage
  • symptoms start early in life and high rate of spontaneous gene mutations responsible (30%)
  • lab: normal bleeding time, prolonged PTT, decreased VIII <1% severe cases
  • replacement VIII
  • complications: joint disease, pseudotumors, fatal hemorrhage
  • therapy complications- transfusion-transmitted diseases, formation of antibodies to transfused VIII, allergic rxn
33
Q

What are the characteristics of Hemophilia B?

A
  • X recessive
  • decreased production of IX
  • similar to VIII deficiency, mild cases hard to diagnose
  • lab: low levels of IX
  • complications: similar to VIII
34
Q

What are the characteristics of thrombocytopenia?

A
  • clinical: petechial hemorrhages in skin and mucous membranes
  • conditions arising from this: sepsis, DIC, TTP, vasculitis, burns, fat emboli, hemorrhage
35
Q

What are the characteristics of Immune Thrombocytopenic Purpura?

A
  • also ITP
  • immune-mediate destruction of platelets, directed at the platelet membrane antigens
  • Acute- in childhood resulting in severe thrombocytopenia- self limiting
  • Chronic- in adults onset gradual, no antecedent infection, females with autoimmune disorders predominate
  • increased risk of bleeding, petechial hemorrhage, bruising
  • therapy: corticosteroids, intravenous antibodies, splenectomy
36
Q

What are the characteristics of Thrombotic Thrombocytopenic Purpura?

A
  • intravascular platelet activation with formation of platelet-rich microthrombi throughout circulation
  • deficient in MMP that normally degrades very high molecular weight multimmers of vWF
  • results in accumulation of abnormally large vWF in plasma
  • high mortality
  • fever, thrombocytopenia, renal failure, microangiopathic hemolytic anemia
  • lab: thrombocytopenia, schistocytes in peripheral blood smear, reticulocytosis; normal coag parameters, increased bilirubin and LD
37
Q

What are the characteristics of DIC?

A
  • uncontrolled activation of hemostatic system, systemic thrombin formation and systemic plasmin formation
  • coag factors consumed resulting in bleeding and microvascular thrombi
  • Clinically things that can cause DIC- bleeding from multiple sites, hypotension, shock, disfunction of things that need blood, gram negative sepsis
  • therapy- remove initiating stimulus, support coag factor reserve
38
Q

Vascular injury exposes

A

subendothelial collagen, which results in platelet activation (primary hemostatic plug), followed by activation of coagulation proteins to produce a more stable meshwork associated with the platelet plug to seal off the damaged site and prevent further blood loss

Gen Path Exam 2 (12 decks)

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