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ACVS Phase I > Tobias Chapter 7 - Bleeding and Hemostasis > Flashcards

Tobias Chapter 7 - Bleeding and Hemostasis Flashcards

1
Q

Define primary and secondary hemostasis

A

Primary hemostasis: the interaction between platelets and endothelium, resulting in the formation of a platelet plug. Secondary hemostasis: a sequence of proteolytic reactions involving coagulation factors, and resulting in the production of fibrin polymers, which stabilize the platelet plug to form a mature thrombus.

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2
Q

What is the definition and importance of fibrinolysis?

A

Fibrinolysis refers to the process of fibrin dissolution to restore vascular patency. This process occurs concomitantly with the two phases of coagulation and is integral to the maintenance of vascular supply through controlled coagulation.

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3
Q

What is the lifespan of platelets in dogs and cats?

A

1 week

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4
Q

What is the sequence of events during the activation of the Cascade model of coagulation? What starts each of the two branches of this cascade?

A

The cascade model proposes the existence of an intrinsic and extrinsic pathways, either of which can lead to the formation of fibrin, the end product of coagulation. INTRINSIC: factor 12 (Hagen/kallikrin);. EXTRINSIC: Tissue factor. Either leads to conversion of factor X to Xa > V to Va > Prothrombin to thrombin > Fibrinogen to Fibrin

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5
Q

What are the three phases of the cell-based model of coagulation?

A

Initiation, amplification and propagation

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6
Q

What are the events of the initiation phase of the cell based model of coagulation?

A

Vascular damage leads to exposure of tissue factor (TF) to plasma. TF activates factor VII to VIIa > X to Xa > Small amounts of thrombin (II to IIa)

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7
Q

What are the events of the amplification phase of the cell-based model of coagulation?

A

Thrombin amplifies the initial signal by activating platelets and cofactors (fVa, fVIIIa) on the platelet surfaces (priming, or amplification phase)

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8
Q

What are the events of the propagation phase of the cell-based model of coagulation?

A

Platelets express large amounts of high affinity coagulation receptors on their surface, leading to large scale thrombin production.

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9
Q

The cell based model of coagulation offers a more logical explanation of the mechanism that regulates coagulation. Explain.

A

The cell-based model assigns activation and propagation to different cell components. Tissue Factor, necessary for the initiation phase, is not present in platelets. Non-activated platelets, a component of the amplification phase, do not express the necessary surface (procoagulant membrane) to activate sufficient amount of prothrombin.

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10
Q

What does “platelet activation“ mean at a membrane level?

A

Non-activated platelets expose neutral phospholipids to the outer surface of the cell membrane. Upon activation, these phospholipids are shuffled to expose the negatively charged end to the outer surface of the cell. The negatively charged surface is able to activate coagulation factors, thereby “amplifying” the coagulation process.

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11
Q

What are the three inhibitors utilized by the endothelium to control platelet activation? What is their basic function?

A

Prostacyclin (PGI2 - produced from Arachidonic to Acid through COX2 > limits TXa2 action)
Ecto-ADPase (metabolizes ADP produced by platelets, preventing activation)
Nitric Oxide (produced by nitric oxide, synthesis, diffuses into platelets and decreases intracellular, calcium, decreasing the expression of integrin and affinity for fibrinogen binding sites.

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12
Q

What are the three natural anticoagulant pathways? What is their function?

A

Antithrombin: binds and inactivates coagulation proteins that escape the site of injury, particularly thrombin (IIa) and Xa.
Protein C: inactivates factors Va and VIIa
Tissue factor pathway inhibitor: binds and inactivates factor Xa

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13
Q

Describe the basic structure of the fibrinolytic system

A

Plasminogen activators (Tissue-kind and Urokinase-kind, t-PA and u-PA) convert plasminogen into plasmin, which degrades fibrin into fibrin degradation product (FDP’s). T-PA is produced by the endothelium, and requires fibrin as a co-factor, therefore the reduction in fibrin availability prevents excessive plasma agent conversion.

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14
Q

How is fibrinolysis controlled? What is the primary inhibitor?

A

Plasminogen Activator Inhibitor-1 inhibits both t-PA and u-PA; stored in platelet alpha granules, and released upon platelet activation.

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15
Q

What is pseudothrombocytopenia? When is this likely to occur and in what species is most commonly observed?

A

Artifact observed when platelets are not adequately counted by the automated analytical process. Most commonly observed in cats (71%) due to the similarity in size between RBCs and platelets.

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16
Q

How can an estimate of platelet count be made based on a blood smear? What is the main limitation to this method?

A

If clumping is not present(limitation), the platelet count can be estimated. This is achieved by multiplying the average number of platelets per high-power field (within the monolayer of the blood film) by 15,000.

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17
Q

What does the Buccal mucosal bleeding time assess? For what conditions is it indicated?

A

Primary hemostasis. Indicated for cases of suspected thrombocytopenia, thrombopathia and vasculopathy.

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18
Q

What do PT and aPTT assess? Which is more sensitive to Factor VII deficiency and why?

A

Both assess secondary hemostasis. PT (prothrombin time): extrinsic and common pathways. Sensitive to factor VII deficiency (very short half-life) / aPTT (activated partial thromboplastin time): intrinsic and common pathways.

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19
Q

Are PT/APTT good tests to predict whether or not a patient will develop significant hemorrhage during a surgical procedure?

A

No. They assess in vitro coagulation based on the cascade model, which does not correlate well with in vivo hemostasis. They are particularly useful for identifying deficiencies in secondary hemostasis, which would be more relevant in the post operative period.

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20
Q

What does Activated Clotting Time (ACT) assess? How does it compare with the most commonly utilized tests in clinical practice?.

A

ACT assesses the intrinsic and common pathways via activation of factor XII. Significantly less sensitive than aPTT.

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21
Q

How are Fibrin Degradation Products (FDP’s) produced? Are they detrimental?List three conditions that may lead to high levels of FDP’s.

A

FDP’s are produced when plasma, degrades, fibrinogen, soluble fibrin, and cross-link fibrin. High levels increase fibrinogenolysis and fibrinolysis, impairing coagulation. Maybe observed in SIRS, IMHA and Sepsis.

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22
Q

What are D-dimers? What is their clinical use?

A

D-dimers are degradation products of cross-linked fibrin. They are not only reflective of activation, like FDP‘s, but rather reflective of ongoing coagulation and fibrinolysis. Sensitive indicator of DIC and thromboembolism, but are not specific. Not sensitive in cats.

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23
Q

List three factors that inhibit fibrin polymerization

A

Heparin, FDP’s and Hypoalbuminemia.

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24
Q

How is the fibrinogen assay clinically useful if PT/ APTT essays are commonly available? How is this test performed?

A

PT/APTT assess the coagulation cascade that will result in the formation of a fibrin clot. These tests, however, will not be significantly prolonged until fibrinogen levels are quite depleted (less than 50 to 100 mg/dL) Fibrinogen is measured as “functional fibrinogen”, which is the time taken for a standard thrombin solution to convert fibrinogen into fibrin.

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25
Q

What are the four phases of coagulation according to the cell based model?

A

Activation, amplification, propagation, and fibrinolysis

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26
Q

How does thromboelastography compare with routine coagulation tasks in the clinical setting? Respond using positive and negative predictive values for bleeding

A

Thromboelastography more closely correlates with clinical bleeding than routine clotting tests (PT, aPTT). Thromboelastography has a positive predictive value of 89% and negative predictive value of 98% for bleeding routine coagulation tests have a positive predictive value of 50% and negative predictive value of 81%

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27
Q

What factors can adversely affect the results of thromboelastography? How

A

Red blood cell mass negatively affect the results. Anemia leads to falsely hypercoagulable results. Polycythemia leads to falsely hypocoagulable results.

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28
Q

Evans syndrome is a potential primary bleeding disorder. What does this syndrome entail?

A

Immune-mediated thrombocytopenia and immune-mediated hemolytic anemia

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29
Q

Disorders of primary hemostasis include causes of decreased platelet production. List five differentials.

A

Immune-mediated Megakaryocytic hypoplasia, retroviral infection (FIV/FeLV), estrogen- related bone marrow suppression, myeloproliferative disease, myelodysplasia, radiation, infection (Anaplasma platis), drug induced.

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30
Q

Disorders of primary hemostasis include causes of increased destruction of platelets. List five differentials.

A

Primary Immune-mediated thrombocytopenia: Idiopathic, Evans syndrome (ITP + IMHA), SLE. Secondary Immune-mediated thrombocytopenia: drugs, tick-borne disease, neoplasia, live virus vaccines

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31
Q

Disorders of primary hemostasis include causes consumption or sequestration of platelets. List five differentials.

A

Disseminated intravascular coagulation, microvascular disease, splenic torsion, severe bleeding, sepsis, hypothermia, severe uremic syndrome.

32
Q

Thrombopathias can be acquired or inherited. List 3 examples of each.

A

Acquired thrombopathia: Drug-induced (NSAID, Sulfonamide Abx, heparin), anemia, uremia, hypothermia, colloid hemodilution, DIC / Inherited thrombopathia: von Willebrand disease (many dog breeds, rare in cats), Signal transduction disorders (Basset Hound, Spitz), Glanzmann’s thrombasthenia (Otterhound, Great Pyrenees)

33
Q

Disorders of primary hemostasis can be caused by vascular abnormalities. List three differentials.

A

Vasculitis, Cushing’s disease, atherosclerosis, Ehlers-Danlos syndrome

34
Q

His orders of secondary hemostasis can be acquired or inherited. List three differentials for each.

A

Acquired: vitamin K deficiency, hepatic disease, acidemia, DIC, shock, massive trauma. Inherited: I: Hypofibrinogenemia and dysfibrinogenemia (Bernese Mountain Dog, Borzoi, Lhasa Apso, Vizsla, Saint Bernard, other dog breeds); II: Hypoprothrombinemia (Boxer, Otterhound, English Cocker Spaniel), VIII: Hemophilia A (German Shepherd Dog, other dog breeds, mixed-breed dogs, cats), IX: Hemophilia B (numerous dog breeds, cats)

35
Q

You are presented with a miniature poodle known to have a factor XII deficiency. Are you concerned about taking the patient to surgery?

A

No, Hageman factor deficiency is a non-pathologic inherited disorder of secondary coagulation.

36
Q

What are the three clinical findings in a polytrauma patient collectively known as “trial of death“

A

Coagulopathy, hypothermia, acidosis

37
Q

What are the three hypothesis that attempt to explain the occurrence of acute traumatic coagulopathy?

A

Disseminated intravascular coagulation with a hyperfibrinolytic phenotype / Enhanced thrombomodulin-thrombin protein C pathway / Catecholamine-induced endothelial damage

38
Q

DIC is usually a hypercoagulable condition, yet it is associated with acute traumatic coagulopathy. How so?

A

In the first 24 to 48 hours, DIC leads to excessive conversion of prothrombin into thrombin, leading to hyperfibrinolysis. This effect is compounded by inhibition of plasminogen activator inhibitor 1.

39
Q

What is the sequence of events linking tissue injury and acute traumatic coagulopathy?

A

Tissue injury leads to exposure of subendothelial collagen and vWF > VIIa-VII > Xa-X>IIa (prothrombin)) - II (thrombin). Thrombin binds to thrombomodulin, activating Protein C (anticoagulant) > inhibits Plasminogen Activator Inhibitor 1(PAI-1)

40
Q

How does inflammation affect coagulation?

A

Inflammation leads to the production of TNF-α, interleukin [IL]-1, IL-6 and chemokines, and the activation of complement pathways, promoting both coagulation and hyperfibrinolysis. The end result (thromboembolism/coagulopathy) will depend on the stage of the process.

41
Q

How does acidemia affect coagulation? What is a possible clinical scenario in a trauma case, and what is the potential effect of buffer administration?

A

pH below 7.2 decreases the activity of factors Xa-Va by 50%. This is common after large blood transfusions , and is not reversed by the administration of buffers.

42
Q

How does hypothermia affect coagulation?

A

Decreases platelet-vWF adhesion

43
Q

How does hemodilution affect coagulation? What is the most common resuscitation fluid associated with this effect?

A

During blood loss, the synthesis of fibrinogen cannot compensate for the rapid loss. Hemodilution horses that scarcity of fibrinogen, which is the most important coagulation factor. At levels below 50 mg/dl clot formation does not occur. Hetastarch has the most pronounced effect because it affects not only fibrinogen but also vWF and Factor VIIIs.

44
Q

Anemia is a common finding a critical patient and can predisposed to coagulopathy. What is the role of red blood cell in coagulation?

A

Relet cells are believed to facilitate dispersion of platelets towards the periphery of blood vessels, facilitating contact with subendothelial factors (collagen, tissue factor, and vWF). This enhances platelet release of ADP and TXA, and facilitates the scavenging of nitric oxide.

45
Q

Routine regulation tests include platelet count, PT and APTT when would you also recommend a buccal mucosal bleeding time?

A

In a patient with suspected thrombopathia, such as von Willebrand’s disease, patients receiving drugs that may alter platelet function (NSAID, sulfonamide Abx).

46
Q

Will thromboelastography detect coagulopathy secondary to von Willebrand disease?

A

No

47
Q

What are the typical clinical signs associated with primary coagulation disorders?

A

Petechiation (more common with thrombocytopenia then with thrombopathia), echimosis, epistaxis, hyphema, hematuria, melena.

48
Q

What clinical findings are common inpatients with disorders of secondary graduation?

A

Hematomas, intra-cavitary bleeding, hemarthrosis.

49
Q

What percentage of blood loss can a patient sustain while still maintaining normotension?

A

40%

50
Q

You performed a splenectomy in a case of Hemoabdomen two hours ago, and the patient is now presenting clinical signs compatible with ongoing hemorrhage. You request a thromboelastogram which yields normal results. What do you do?

A

Thromboelastogram results should be prolonged in the postoperative period. Normal results in the face of bleeding indicate a technical cause for hemorrhage, and require immediate surgical intervention (97% predictive value)

51
Q

What is Trauma Induced Hypercoagulability (TIC)?

A

TIC is a lethal, unbalanced, and abnormal coagulation process. Its early stages are characterized by hypercoagulability and bleeding whereas the later stages are characterized by hypercoagulability with venous thromboembolism and multiple organ failure.

52
Q

What is the main indication for fresh frozen plasma?

A

Replacement of all coagulation factors in patients with inherited or acquired secondary coagulation disorders. Includes vWF.

53
Q

What clotting factors does frozen plasma contain?

A

II, VII, IX and X

54
Q

What does cryoprecipitate contain?

A

vWF, VII, fibrinogen and fibronectin

55
Q

What is the preferred blood product for the treatment of von Willebrand’s disease?

A

Cryoprecipitate

56
Q

What is the recommended threshold for platelet transfusion in a patient about to undergo a surgical procedure? (derived from human literature).

A

50,000 cells/ul

57
Q

What is desmopressin? What is its clinical use?

A

Desmopressin [DDAVP]) is a synthetic vasopressin analogue that induces, via V2 receptors, the release of subendothelial vWF stores. It acts to increase platelet function by enhancing the release of not only vWF, but also factor VIII and plasminogen from the endothelium.

58
Q

What are the limitations associated with the use of desmopressin in patients with type 1 von Willebrand‘s disease?

A

The onset of action is delayed by 30 minutes. Effect lasts 2 hours. Repeated doses may lead to vWF depletion.

59
Q

Aminocaproic acid and Tranexamic acid are commonly utilized in patients with suspected hyperfibrinolysis. How do these drugs work?

A

Both drugs are lysine analogues that block the conversion of plasminogen into plasmin. They also possess anti-inflammatory effects through inhibition of interleukins.

60
Q

What dog breed is frequently linked with non-pathologic thrombocytopenia?

A

Cavalier king Charles spaniel

61
Q

What are the functions of von Willebrand’s factor? List three breeds predisposed the type one von Willebrand’s disease.

A

vWF facilitates platelet adhesion to the subendothelium as well as platelet aggregation by binding factor VIII. Doberman Pincher, Standard Poodle, German Shepherd, Airedale Terrier.

62
Q

What are the three forms of von Willebrand’s disease?

A

Type 1: most common form; all multimers present, but in reduced concentration. Bleeding not observed until vWF <20% / Type 2: least common form; relative deficiency of high molecular weight multimers. / Type 3: most severe form, characterized by complete absence of all multimers. Life-threatening hemorrhage likely to occur.

63
Q

You have a patient with type one von Willebrand disease who will undergo surgery in a few hours. What recommendations would you make to improve this patients coagulation status?

A

Desmopressin administration (lasts 2 hours) and Cryoprecipitate transfusion 30 minutes before surgery (last 4 hours)

64
Q

What is the Virchow’s triad?

A

Defines thromboembolic tendency. Virchow’s triad: abnormalities of the vessel wall (endothelial injury), abnormalities of blood flow (vascular stasis), and abnormalities of blood constituents that promote hemostasis (hypercoagulability).

65
Q

How does hypoalbuminemia increase a patient’s risk to thromboembolism?

A

Hypoalbuminemia increases TxA2 production, enhancing platelet aggregation.

66
Q

List five conditions commonly associated with a hypercoagulable state

A

IMHA, pancreatitis, PLN, PLE, sepsis, SIRS

67
Q

What lung lobes are most commonly affected in cases of pulmonary thromboembolism?

A

Right middle and caudal lobes

68
Q

What laboratory test is indicated in a case of suspected pulmonary thromboembolism in a dog?

A

D-dimers

69
Q

What is the mechanism of action of unfractioned heparin?

A

Potentiates antithrombin activity, inactivating thrombin and factor Xa

70
Q

Aspirin can be used to prevent thromboembolism. What is the mechanism of action?

A

Aspirin induces an irreversible inhibition of COX-1, leasing to suppression on TxA2 synthesis. This prevents platelet aggregation for the duration of the platelets life.

71
Q

Inflammation and coagulation are tightly interconnected. List three cytokines responsible for this connection.

A

IL-1, IL-6, TNF-alpha

72
Q

Diagnosis of DIC can be challenging and is typically based on the presence of underlying hypercoagulable condition as well as three or more laboratory abnormalities. List them.

A

thrombocytopenia, prothrombin time (PT) and/or activated partial thromboplastin time (APTT) prolongation, elevated levels of fibrin split products or D-dimers, hypofibrinogenemia, reduced antithrombin activity, and/or red blood cell fragmentation.

73
Q
A
74
Q

What does this diagram represent? Define R, K, Alpha, MA and LY-60

A

Thromboelastogram. The thromboelastography tracing (thromboelastogram) provides a visual representation of hemostasis. The reaction time (R) represents the time of latency from test initiation until beginning of fibrin formation, measured as an increase in amplitude of 2 mm. The clotting time (K) is the time to clot formation, measured from the end of R until an amplitude of 20 mm is reached. The angle (α) represents the rapidity of fibrin accumulation and cross-linking. Maximum amplitude (MA) represents clot strength. LY60 reflects fibrinolysis, determined by the percentage decrease in amplitude 60 minutes following MA. PT, Prothrombin time; PTT, partial thromboplastin time; TF, tissue factor

75
Q

What do the following TEG profiles represent, and how would you treat them?

A

ACVS Phase I (7 decks)

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