Coagulation/Platelets Flashcards
At low shear conditions, which of the following substances is NOT important for platelet adhesion:
a. Collagen
b. Thrombin
c. Fibronectin
d. Laminin
b. Thrombin
c. Fibronectin
d. Laminin
The following inherited platelet disorder is NOT reported to have abnormal clot retraction times:
a. Cyclic hematopoiesis
b. Chediak-Higashi syndrome
c. CalDAG-GEFI syndromes
d. Glanzmann thrombasthenia
C. Normal clot retraction occurs in the CalDAG-GEFI platelet disorders (canine thrombopathias)
because these platelets can interact with thrombin and express fibrinogen receptors.
Endothelial cells express substances on the surface that degrade platelet agonists, and synthesize inhibitors of platelet activation. Which of the following substances inhibits platelet activation?
a. Prostacyclin
b. ADP
c. Thrombin
d. Fibrinogen
a. Prostacyclin
When stimulated by [ADP, thromboxane, thrombin and PAF (platelet activating factor)] endothelial cells produce prostacyclin
The following is most true regarding platelet hypofunction due to anti-platelet antibodies:
a. Antibodies are usually directed at platelet DNA.
b. Antibodies are usually directed at membranous proteins, including GPIIb-IIIa.
c. Antibodies are directed at RBC antigens (Ag’s) and cross react with platelet Ag’s.
d. Antibody mechanisms are not exploited with drugs such as Plavix.
b. Antibodies are usually directed at membranous proteins, including GPIIb-IIIa.
reduced function may be explained by the finding that GPIIb/IIIa (fibrinogen receptor) and GPIb-IX (part of vWF receptor complex) are the most frequently targeted antigens
Anti-inflammatory agents inhibit platelet function through:
a. Activation of the cyclooxygenase (COX) enzyme system.
b. Inactivation of the COX enzyme system.
c. Increasing the amount of thromboxane A2 (TXA2)
d. Ablation of the COX enzymes and their related proteins.
b. Inactivation of the COX enzyme system.
The most common inherited intrinsic platelet disorder in dogs, and possibly other species, is characterized by a decrease to absent response to most platelet-activating agents, including ADP and collagen. What is the molecular bases for these disorders?
a. Mutation in the platelet ADP receptor P2Y12.
b. Mutation in the gene encoding adaptor protein complex 3 (AP3) beta-subunit
c. Mutation within the gene sequence that encode highly conserved calcium-binding domains within the GPIIb.
d. Mutation in the gene encoding calcium diacylglycerol guanine nucleotide exchange factor I (CalDAG-GEFI)
a. Mutation in the platelet ADP receptor P2Y12.
Which one of the following factors is involved in preventing platelet adherence to normal endothelial cells?
a. ADPases
b. Heparan sulfate
c. Prostacyclin
d. Thrombomodulin
a. ADPases
can degrade ADP released from activated platelets
Which one of the following factors mediates platelet aggregation only in low shear conditions?
a. Adenosine diphosphate (ADP)
b. Fibrinogen
c. Thrombin
d. Von Willebrand Factor (vWF)
a. Adenosine diphosphate (ADP)
b. Fibrinogen
c. Thrombin
????
High shear forces
Von Willebrand Factor (vWF)
Which of the following intrinsic platelet disorders also affect melanocytes? I. Glanzmann Thrombasthenia II. Chediak-Higashi Syndrome III. Cyclic Hematopoiesis IV. Scott Syndrome
A. I and II B. I and III C. II and III D. I, III, and IV E. I, II, III, and IV
C.
II. Chediak-Higashi Syndrome
III. Cyclic Hematopoiesis
All of the following contribute to platelet antagonism EXCEPT:
a. Erythropoietin
b. Heparan Sulfate
c. Thrombomodulin
d. Liver Insufficiency
a. Erythropoietin
All of the following contribute to the anti-thrombotic activity of the endothelium EXCEPT:
a. Nitric Oxide
b. Prostacyclin
c. Thrombomodulin
d. von Willebrand Factor
d. von Willebrand Factor
Type 1 Von Willebrand Disease is characterized by which of the following:
a. An equal decrease in all sizes of multimers of VWF
b. A decrease in only the large multimers of VWF
c. A decrease in only the small multimers of VWF
d. An absence of all multimers of VWF
a. An equal decrease in all sizes of multimers of VWF
A decrease in only the large multimers of VWF - TYPE II
An absence of all multimers of VWF = TYPE III
Which of the following platelet agonists are not synthesized de novo within platelets upon activation?
a. TXA2
b. 12-HETE
c. PAF
d. ADP
a. TXA2
Cyclic Hematopoesis is an inherited thrombocytopathia which results from which of the following platelet defects?
a. ADP receptor malformation
b. Failure of activation of β integrins
c. Lack of dense granules
d. β-tubulin defect/malformation
c. Lack of dense granules
ADP receptor malformation - P2Y12 gene
Failure of activation of β integrins - Kindlin-3 Disorder
β-tubulin defect/malformation - hereditary macrothrombocytopenia
Under low shear conditions, platelet adhesion to the subendothelium occurs via which of the following:
a. collagen , VWF, and fibronectin
b. collagen, laminin
c. collagen, VWF
d. collagen, fibronectin and laminin
a. collagen , VWF, and fibronectin
The gene defect responsible for several signal transduction disorders, including Basset hound, Landseer-ECT, and bovine thrombopathias, is:
a. CalDAG-GEFI
b. P2Y12
c. beta 1 tubulin
d. Kindlin 3
a. CalDAG-GEFI
Fibrin degradation products are removed from the body via:
a. splenic macrophages
b. filtration at the glomerulus
c. hepatic macrophages (Kupffer cells)
d. biliary excretion
c. hepatic macrophages (Kupffer cells)
Thrombopoeitin is responsible for stimulating platelet synthesis in the bone marrow. Which of the following is true regarding thrombopoeitin?
a. Thrombopoeitin is made only in the bone marrow and smooth muscle cells.
b. Thrombopoeitin production is upregulated in response to low platelet numbers.
c. Thrombopoeitin is regulated through a positive feedback mechanism.
d. Thrombopoeitin is cleared from circulation by adsorption onto platelets.
d. Thrombopoeitin is cleared from circulation by adsorption onto platelets.
During high shear conditions, which factors mediate platelet adhesion to subendothelial connective tissue?
a. Fibrinogen and GPIIb-IIIa
b. VWF, GPIb-IX-V complex, and collagen
c. Collagen, fibronectin, and laminin
d. VWF and GPIb-IX-V complex
d. VWF and GPIb-IX-V complex
Chediak Higashi syndrome is characterized by:
a. Absent or reduced expression of GPIIb-IIIa
b. A mutation in the gene encoding CalDAG-GEFI
c. Absence of dense granules in platelets
d. Failure of activation of β1, β2, and β3 type integrins
c. Absence of dense granules in platelets
All of the following substances are found in dense granules except.
a. ATP
b. ADP
c. Fibrinogen
d. Calcium ions
c. Fibrinogen
The mutation of what gene is associated with signal transduction disorders?
a. KINDLIN3
b. CalDAG-GEFI
c. P2Y12
d. P2Y
b. CalDAG-GEFI
In what disease will you see normal platelet function, but secondary hemostasis is affected because of an inability of express phosphatodylserine (PF3, PCA) or prothrombase on the surface of the platelet?
a. Beta tubulin deficiency
b. Dense Granule Defect
c. Scott’s Syndrome
d. Chediak- Higahi Syndrome
c. Scott’s Syndrome
What is the next step in hemostasis after platelets attach to the endothelium via vWF and collagen?
a. Prostacyclin is released from the platelet
b. The platelet undergoes a conformational change, exposing Integrin αIIbβ3
c. Dense granules release ADP, ATP, and histamine
d. Plasminogen is activated to plasmin
b. The platelet undergoes a conformational change, exposing Integrin αIIbβ3
All of the following conditions are associated with causing decreased platelet function except:
a. Liver disease
b. Immune mediated thrombocytopenia
c. Neoplasia
d. BETA1-Tubulin macrothrombocytopenia
a. Liver disease
In regards to extrinsic and intrinsic platelet disorders, which of the following statements is true?
a. Intrinsic disorders have normal platelets, but a protein associated with platelet function is either reduced, absent, or non-functional. An example of this is von Willebrand’s disease.
b. Intrinsic disorders involve the defects in the platelets directly, such as defects in granules, membrane glycoproteins, or signal transduction proteins. An example of this is cyclic hematopoiesis.
c. Extrinsic disorders involve the defects in the platelets directly, such as defects in granules, membrane glycoproteins, or signal transduction proteins. An example of this is Chediak-higahi syndrome.
d. Extrinsic disorders have normal platelets, but a protein associated with platelet function is either reduced, absent, or non-functional. An example of this is the dense granule defect seen in Cocker Spaniels.
a. Intrinsic disorders have normal platelets, but a protein associated with platelet function is either reduced, absent, or non-functional. An example of this is von Willebrand’s disease.
b. Intrinsic disorders involve the defects in the platelets directly, such as defects in granules, membrane glycoproteins, or signal transduction proteins. An example of this is cyclic hematopoiesis.
c. Extrinsic disorders involve the defects in the platelets directly, such as defects in granules, membrane glycoproteins, or signal transduction proteins. An example of this is Chediak-higahi syndrome.
d. Extrinsic disorders have normal platelets, but a protein associated with platelet function is either reduced, absent, or non-functional. An example of this is the dense granule defect seen in Cocker Spaniels.
In the most common type of Von Willebrand Disease in dogs, what are the qualitative and/or quantitative changes in the VWF multimers?
a. Decreased number of small multimers
b. No detectable multimers
c. Decreased number of all of the multimers, with detectable presence of the multimers
d. Decreased number of large multimers with concurrent qualitative dysfunction of the multimers
c. Decreased number of all of the multimers, with detectable presence of the multimers
Which of the following factors play a role in both low shear and high shear platelet activation and is the most potent activator of platelets?
a. Thrombin
b. ADP
c. TXA2
d. Epinephrine
a. Thrombin
b. ADP
c. TXA2
d. Epinephrine
Proteins S and C are synthesized by:
a. platelets
b. endothelium
c. macrophages
d. liver
d. liver
Adhesion molecules on platelets, leukocytes, and endothelial cells can be up regulated by protease activated receptors (PARS) that are activated by:
a. Thrombin, V and TF-VII
b. Thrombin, X and TF-VII
c. Thrombin, V and X
d. Thrombin, V, X, and TF-VII
a. Thrombin, V and TF-VII
b. Thrombin, X and TF-VII
c. Thrombin, V and X
d. Thrombin, V, X, and TF-VII
- In what platelet disorder will there be normal platelet function testing (including buccal mucosal bleeding time, platelet aggregation, and TEG) and clinical signs consistent with a coagulopathy?
a. Von Willebrand Disease
b. Cyclic hematopoiesis
c. Scott syndrome
d. Kindlin-3 disorders
c. Scott syndrome
Important factors that influence TEG coagulation results, outside of the actual coagulation status of the patient, include all of the following EXCEPT:
a. hematocrit
b. activator type
c. heparin therapy
d. activator concentration
b. activator type
d. activator concentration
The activity of which enzyme is required to regenerate Vitamin K:
a. Alkaline Phosphatase
b. Aldehyde dehydrogenase
c. Vitamin K Carboxylase
d. Vitamin K epoxide reductase
d. Vitamin K epoxide reductase
The three components of the “lethal triad” that are known to exacerbate the condition known as Acute Traumatic Coagulopathy include:
a. Hypothermia, Acidosis, Coagulopathy
b. Hypothermia, Alkalosis, Coagulopathy
c. Hyperthermia, Acidosis, Coagulopathy
d. Hyperthermia, Alkalosis, Coagulopathy
a. Hypothermia, Acidosis, Coagulopathy
Palmer, L., Martin, L. (2014), Traumatic Coagulopathy – Part 1: Pathophyciology and Diagnosis. Journal of Veterinary Emergency and Critical Care. 24(1): p.68
Of the Thromboelastography tracings below, (A) is normal. What is the most likely explanation for (B - appears to clot initially, but then tapers off)?
a. Thrombocytopenia
b. Fibrinolysis
c. Factor X deficiency
d. DIC
b. Fibrinolysis
VPB8434 Coagulation Lecture powerpoint, Dr. Angela Royal on 30 OCT 2014
Which of the following vertebrates have both thrombocytes and platelets been noted in certain species:
a. Birds
b. Reptiles
c. Amphibians
d. Fish
c. Amphibians
Campbell, T. W., Ellis, C. K. Avian and Exotic Animal Hematology and Cytology. 3rd Ed. Iowa: Blackwell Publishing. 2007. p. 89
Which one of the following is NOT a current hypothesis to explain the pathophysiological mechanism underlying clinical manifestation of acute traumatic coagulopathy?
a. Disseminated intravascular coagulation with a fibrinolytic phenotype
b. Enhanced activation of the thrombomodulin-thrombin protein C anticoagulant pathway
c. Loss, consumption and dilution of hemostatic factors or platelets
d. Marked sympathoadrenal response leading to catecholamine-induced endothelial damage
c. Loss, consumption and dilution of hemostatic factors or platelets
Palmer L, Martin L. Traumatic coagulopathy-Part 1: Pathophysiology and diagnosis. J Vet Emerg Crit Care. 2014 Jan-Feb;24(1):63-74. (p. 65)
According to the PROVETS guidelines on rotational viscoelastic assays in veterinary medicine, which one of these recommendations is true regarding sample collection and handling?
a. Blood should be collected using evacuated tubes exclusively.
b. Consistent venipuncture site should be used if serial samples are compared.
c. Samples should be stored at 37°C for 30 minutes prior to analysis.
d. When multiple tubes are drawn, citrate tube should be obtained first.
b. Consistent venipuncture site should be used if serial samples are compared.
Goggs R, Brainard B, de Laforcade AM, Flatland B, Hanel R, McMichael M, Wiinberg B. Partnership on Rotational ViscoElastic Test Standardization (PROVETS): Evidence-based guidelines on rotational viscoelastic assays in veterinary medicine. J Vet Emerg Crit Care. 2014 Jan-Feb;24(1):1-22. (p. 4)
According to the PROVETS guidelines on rotational viscoelastic assays in veterinary medicine, there is insufficient evidence to recommend how to define hemostatic abnormalities based on TEG/ROTEM parameters; however, trends in variables have been suggested. Which one of these abnormalities currently can NOT be detected by standard TEG/ROTEM parameters?
a. Hypercoagulability
b. Hypocoagulability
c. Hyperfibrinolysis
d. Hypofibrinolysis
d. Hypofibrinolysis
Goggs R, Brainard B, de Laforcade AM, Flatland B, Hanel R, McMichael M, Wiinberg B. Partnership on Rotational ViscoElastic Test Standardization (PROVETS): Evidence-based guidelines on rotational viscoelastic assays in veterinary medicine. J Vet Emerg Crit Care. 2014 Jan-Feb;24(1):1-22. (p. 12)
What is the recommended blood collection method for viscoelastic testing?
a. Jugular venipuncture with blood tube collection in the following order: discard/serum tube, citrate tube, EDTA tube, and heparin tube.
b. Jugular venipuncture with blood tube collection in the following order: heparin tube, EDTA tube, citrate tube, and discard/serum tube.
c. Cephalic venipuncture with blood tube collection in the following order: EDTA tube, heparin tube, citrate tube, and discard/serum tube.
d. Saphenous venipuncture with blood tube collection in the following order: citrate tube, serum/discard tube, EDTA tube, and heparin tube.
a. Jugular venipuncture with blood tube collection in the following order: discard/serum tube, citrate tube, EDTA tube, and heparin tube.
Partnership on Rotational ViscoElastic Test Standardization (PROVETS), Robert Goggs, pg. 5.
Complete the following statement with the one best choice.
Antithrombin has anti-inflammatory actions (dependent or independent) of coagulation and can be inhibited by treatment with ________________________, which can lead to decreased survival.
a. dependent, heparin
b. independent, heparin
c. dependent, non-steroidal anti-inflammatory drugs
d. independent, non-steroidal anti-inflammatory drugs
b. independent, heparin
The Reciprocal Relationship Between Inflammation and Coagulation, Mauria O’Brien, pg. 49.
Neutrophil extracellular traps (NETs) can be beneficial and detrimental, which two organs are most commonly damaged by NETS and how are they damaged?
a. The spleen and liver; the endothelium becomes defective after chemotactic mediators initiate neutrophil margination.
b. The kidneys and spleen; the neutrophil proteases expelled by the neutrophils cause mesenchymal necrosis.
c. The liver and lungs; the underlying endothelium becomes damaged after exposure to neutrophil proteases and granular proteins.
d. The lungs and bone marrow; NETs cause an exaggerated inflammatory response resulting in excessive thrombi formation causing coagulative necrosis.
c. The liver and lungs; the underlying endothelium becomes damaged after exposure to neutrophil proteases and granular proteins.
The Reciprocal Relationship Between Inflammation and Coagulation, Mauria O’Brien, pg. 48.
Hemophilia A is a disease of a deficiency in factor
a. FVIII
b. FVII
c. FIX
d. FV
a. FVIII
Reference: Aslanian, M. “Clinical outcome after diagnosis of hemophilia A in dogs”. JAVMA. Pg 677.
Where does the amplification phase of coagulation occur?
a. Platelets
b. Endothelium
c. Red blood cells
d. Fibrin
a. Platelets
The amplification phase of coagulation occurs mainly on platelets. Thrombin activates platelets, and platelet associated factor V. Factor Va acts as a cofactor for factor Xa. Together, they form the prothrombinase complex that convers prothrombin to thrombin and this results in the production of more thrombin. The intrinsic pathway consists of HMWK, pre-kallikrien, and the serine proteases factor XII, factor XI, factor IX, and factor VIII. Thrombin activates FVIII and FXI.
Reference: Kidd. “Prothombotic mechanisms and anticoagulant therapy in dogs with immune mediated hemolytic anemia. JVECCS pg5
Activated platelets and red blood cells release ________, which exposes microparticles.
a. Phosphotidylserine
b. Tissue factor pathway inhibitor
c. Thrombin
d. Plasminogen
a. Phosphotidylserine
Reference: Kidd. “Prothombotic mechanisms and anticoagulant therapy in dogs with immune mediated hemolytic anemia. JVECCS pg 4
Which of the following pairs of factors are globally accepted as main initiators of acute traumatic coagulopathy (ATC)?
A. Tissue injury, hypothermia
B. Systemic inflammation, hemodilution
C. Hypoperfusion, hemodilution
D. Hypoperfusion, tissue injury
D. Hypoperfusion, tissue injury
Palmer and Martin, “Traumatic coagulopathy – part 1” , pg. 67-68
The neurohormonal hypothesis for acute traumatic coagulopathy (ATC) includes which of the following mechanisms?
A. Activation of the protein C anticoagulant pathway
B. Endothelial glycocalyx damage leading to a prothrombotic state
C. Tissue trauma leading to hypoxia
D. Endothelial injury leading to a hypofibrinolytic state
B. Endothelial glycocalyx damage leading to a prothrombotic state
(Palmer and Martin, “Traumatic coagulopathy – part 1” , pg. 66)
According to the PROVET guidelines, which one of the following is currently recommended?
A. All routine TEG assays should be performed at 37 degrees Celsius.
B. The PROVET guidelines should always be followed over manufacturer guidelines.
C. All samples should be refrigerated prior to performing TEG/ROTEM.
D. Samples should never be drawn from intravenous catheters.
A. All routine TEG assays should be performed at 37 degrees Celsius.
(Goggs et al, Partnership on Rotational Viscoelastic Test Standardization (PROVETS), pg. 4-9)
All of the following are contributors to acute traumatic coagulopathy EXCEPT?
a. Tissue injury
b. Hypoperfusion
c. Systemic inflammation
d. Metabolic alkalosis
d. Metabolic alkalosis
Source: Palmer, L and Martin, L. Traumatic coagulopathy-Part 1: Pathophysiology and diagnosis. Journal of Veterinary and Emergency Critical Care. 2014.24(1). Pg. 67.
Which of these statements is true regarding TEG/ROTEM?
a. Recalcification is the ideal way to perform TEG and ROTEM
b. ROTEM only has activators available for the contact pathway
c. ROTEM uses an automated pipetting system to run
d. Hypocoagulable tracings have a shorter initiation time
c. ROTEM uses an automated pipetting system to run
Source: Goggs, R., Brainard, B., et al. Partnership on Rotational ViscoElastic Test Standardization (PROVETS): Evidence based guidelines on rotational viscoelastic assays in veterinary medicine. JVECC. 2014. 24(1). Pg. 1-22.
Which of the following helps to delineate DIC from ATC?
a. Lack of microthrombi formation in ATC
b. ATC has a later onset of action than DIC
c. ATC is associated with clotting factor deficiencies
d. Severe thrombocytopenia is usually seen in ATC
a. Lack of microthrombi formation in ATC
Source: Palmer, L and Martin, L. Traumatic coagulopathy-Part 1: Pathophysiology and diagnosis. Journal of Veterinary and Emergency Critical Care. 2014.24(1). Pg. 65.
Which of the following are NOT a form of viscoelastic hemostasis testing?
A. TEG B. ROTEM C. PTT D. Sonoclot
C. PTT
PPT slide 3 of 9-30-14 Viscoelastic Testing; Royal
If this is a normal TEG tracing:
(image of a normal TEG tracing)
What is this TEG tracing an example of when the R & K are decreased, but the MA and α angle are increased:
(image of a fatter TEG tracing)
A. hemophilia B. platelet blockers C. fibrinolysis D. hypercoagulation
D. hypercoagulation
PPT slide 14 of 9-30-14 Viscoelastic Testing; Royal
What is number of thrombocytes noted in most avian species?
A. 20,000-30,000/μL B. 200,000-300,000/μL C. 2,000-3,000/μL D. 2,000,000-3,000,000/μL
A. 20,000-30,000/μL
pg 578; Schalm’s Veterinary Hematology,6th ed. Weiss & Wardrop, 2010
Which of the following regarding the action of TNF-alpha is true?
A) TNF-alpha inhibits the expression of EPCR and thrombomodulin. B) TNF-alpha increases platelet count C) TNF-alpha increases platelet thrombogenicity D) TNF-alpha suppresses tPA
D) TNF-alpha suppresses tPA
Compendium Box 1 pg E2
Which of the following regarding the action of Thrombin is true.
A) Thrombin decreases NF-kB levels. B) Thrombin stimulates production of platelet activating factor. C) Thrombin decreases the expression of cytokines. D) Thrombin inhibits leukocyte adhesion to endothelial cells.
B) Thrombin stimulates production of platelet activating factor.
(Compendium Box 2 pg E3)
Which of the following regarding Interleukin 6 is true?
A) IL-6 induces tissue factor expression from monocytes. B) IL-6 stimulates the release of PAI-1. C) IL-6 inhibits the expression of EPCR. D) IL-6 Activates factor X
A) IL-6 induces tissue factor expression from monocytes.
compendium Box 1 pg E2
Which of the following correctly describes acute traumatic coagulopathy (ATC)?
a. Occurs <1hr post trauma
b. Occurs after the patient is stabilized (~1-12 hours post trauma)
c. It is a hypocogaulable state with normal fibrinolysis
d. Shares many similarities with DIC including microthrombi development
a. Occurs <1hr post trauma
Page 65 and 72. C) fibrinolysis is increased D) microthrombi are not expected in ATC
Source: Palmer, L. and L. Martin, Traumatic coagulopathy–part 1: Pathophysiology and diagnosis. J Vet Emerg Crit Care (San Antonio), 2014. 24(1): p. 63-74.
Which of the following are proposed mechanisms that contribute to ATC?
I. Systemic inflammation
II. Endothelial damage
III. Shock induced hypoperfusion
IV. Severe tissue injury
a. I, II, IV
b. II, IV
c. III, IV
d. I, III, IV
e. I-IV
e. I-IV I. Systemic inflammation II. Endothelial damage III. Shock induced hypoperfusion IV. Severe tissue injury
Page 72.
Source: Palmer, L. and L. Martin, Traumatic coagulopathy–part 1: Pathophysiology and diagnosis. J Vet Emerg Crit Care (San Antonio), 2014. 24(1): p. 63-74.
Which of the following are the main hypotheses that currently attempt to explain the pathophysiology etiology of ATC?
I. DIC with a fibrinolytic phenotype
II. Sympathoadrenal response leading to catecholamine-induced endothelial damge
III. Hemodilution of coagultion factions from fluid therapy
IV. Thrombin-thrombomodulin activated Protein C pathway
V. Metabolic acidosis leading to decreased activity of hemostatis serine proteases and platelets
a. I, II
b. I, III, V
c. III, V
d. I, II, IV
e. I-V
d. I, II, IV
I. DIC with a fibrinolytic phenotype
II. Sympathoadrenal response leading to
V. Metabolic acidosis leading to decreased activity of hemostatis serine proteases and platelets
Page 65-66. III and V can exacerbate ATC but occur after the onset of ATC andSource: Palmer, L. and L. Martin, Traumatic coagulopathy–part 1: Pathophysiology and diagnosis. J Vet Emerg Crit Care (San Antonio), 2014. 24(1): p. 63-74.
Which of the following is the major mechanism by which antithrombin is decreased in SIRS states?
A) Degradation by elastase from activated neutrophils B) Decreased production by the liver C) Consumption as a result of sustained thrombin generation D) Decreased production of endothelial heparin sulfate proteoglycans (HSPGs)
C) Consumption as a result of sustained thrombin generation
Source: “The reciprocal relationship between inflammation and coagulation,” O’Brien, p. 49
This adhesion molecule mediates leukocyte binding, is found within Weibel-Palade bodies of endothelial cells and activated platelets.
A) P-selectin B) L-selectin C) PECAM-1 D) B1-integrin
A) P-selectin
Source: “The reciprocal relationship between inflammation and coagulation,” O’Brien, p. 47
Which of the following is most consistent with PROVETS guidelines?
A) Each facility needs its own reference interval; citrate tube should be filled before EDTA; 3.2% sodium citrate should be used; sampling from jugular vein is preferred B) One reference interval should be established; tubes can be filled in any order; 3.2% sodium citrate should be used; sampling from jugular vein is preferred C) Each facility needs its own reference interval; citrate tube should be filled before EDTA; 3.8% sodium citrate should be used; sampling from jugular vein is preferred D) Each facility needs its own reference interval; EDTA tube should be filled before citrate tube; 3.8% sodium citrate should be used; sampling from jugular vein is preferred
A) Each facility needs its own reference interval; citrate tube should be filled before EDTA; 3.2% sodium citrate should be used; sampling from jugular vein is preferred
Source: “PROVETS” article, Goggs et al., p. 5
In regards to acute traumatic coagulopathy which of the following is NOT a proposed theory?
A. Endothelial damage from marked catecholamine release
B. Fibrinolytic phenotype of disseminated intravascular coagulation
C. Thrombomodulin-thrombin protein C pathway
D. Deficiency of clotting factors leading to induction of coagulopathy
D. Deficiency of clotting factors leading to induction of coagulopathy
Traumatic coagulopathy-Part 1: Pathophysiology and diagnosis Lee Palmer, DVM, DACVECC and Linda Martin, DVM, MS, DACVECC pg 65
Treatment of acute traumatic coagulopathy often requires large volume resuscitation efforts. Which of the following is NOT one of the complications associated with this treatment?
A. Disruption of formed thrombi
B. Dilution of hemostatic factors
C. Potentiation of hyperthermia
D. Disruption of vasoconstriction
C. Potentiation of hyperthermia
Traumatic coagulopathy-Part 1: Pathophysiology and diagnosis Lee Palmer, DVM, DACVECC and Linda Martin, DVM, MS, DACVECC pg 69
In humans, acute traumatic coagulopathy is commonly defined by the prolongation of aPTT and PT. What is the percent increase that is commonly used?
A. 25%
B. 50%
C. 75%
D. 100%
B. 50%
Traumatic coagulopathy-Part 1: Pathophysiology and diagnosis Lee Palmer, DVM, DACVECC and Linda Martin, DVM, MS, DACVECC pg 69
The following coagulation factor has been designated the main culprit in the activation of coagulation in DIC:
a. Tissue factor
b. Factor VIII
c. Factor X
d. Thrombin
a. Tissue factor
Reference: Stokol, T. “Laboratory diagnosis of Disseminated Intravascular Coagulation in Dogs and Cats: The past, the present, and the future” Vet Clin Small Animal 42 (2012). Pg 190
The factors that make up the lethal triad are hypothermia, coagulopathy, and __________.
a. inflammation
b. tissue injury
c. hemodilution
d. acidosis
d. acidosis
Reference: Palmer L. “Traumatic coagulopathy- Part 1: Pathophysiology and diagnosis” Journal of Veterinary Emergency and Critical Care 24 (1) pp 63 – 74.
This is a disorder of the absence or reduction of GPIIb-IIIa on the surface of platelets. It can be documented in Great Pyrenees, otterhounds, and some horses.
a. Glanzmann thrombasthenia
b. Chediak-Higashi Syndrome
c. Dense Granule Defect
d. Cyclic hematopoiesis
a. Glanzmann thrombasthenia
Reference: Boudreaux, M. “Inherited platelet disorders” Journal of Veterinary Emergency and Critical Care 00 (0) p 1-12
Which platelet receptor does Clopidogrel (Plavix) target?
A) GPIb B) P2Y12 C) GPIIb/IIIa D) PAR1
B) P2Y12
Source: “Assessment of Platelet Function,” Jandrey, JVECC, p. 87
Which platelet analyzer/analysis method evaluates platelet function in a manner similar to buccal mucosal bleeding time (BMBT)?
A) Aggregometry B) Viscoelastic analyzers C) PFA-100 D) Thromboelastography
C) PFA-100
Source: “Assessment of Platelet Function,” Jandrey, JVECC, p. 84
Which cell type, when stimulated, predominantly expresses tissue factor that leads to activation of coagulation during endotoxemia?
A) Monocytes B) Endothelial cells C) Neutrophils D) Platelets
A) Monocytes
Source: “The Reciprocal Relationship Between Inflammation and Coagulation,” O’Brien, Topics in Companion Animal Medicine, p. 47
Which of the following inherited disorders is not associated with the GPIIa/IIIb receptor:
a. Scott Syndrome
b. CalDAG-GEFI
c. Glanzmann’s Thrombasthenia
d. Kindlin-3 Disorder
a. Scott Syndrome
Harvey, J. W. (2012), Veterinary Hematology: A Diagnostic Guide and Color Atlas. St. Louis, MO: Elsevier Saunders, p. 217
A normal platelet count with prolonged PT/PTT and a negative FDP test could indicate which of the following:
a. Generalized bone marrow hypoplasia
b. Rodenticide toxicity
c. Hemophilia A
d. Brachen fern toxicosis
b. Rodenticide toxicity
Harvey, J. W. (2012), Veterinary Hematology: A Diagnostic Guide and Color Atlas. St. Louis, MO: Elsevier Saunders, p. 224
Inflammation and Coagulation are connected through all of the following except for:
a. Activated platelets express P-selectin which binds to PSGL-1 on monocytes, stimulating the release of microparticles
b. Thrombin stimulates the release of various inflammatory cytokines through the NF-κB signaling pathway
c. Anti-thrombin inhibits leukocyte rolling due to the release of prostacyclin and the down modulation of P-selectin
d. Platelets, through PSGL-1, bind LPS and stimulate neutrophils to form neutrophilic extracellular traps (NETs)
d. Platelets, through PSGL-1, bind LPS and stimulate neutrophils to form neutrophilic extracellular traps (NETs)
O’Brien, M. (2012), The Reciprocal Relationship Between Inflammation and Coagulation. Topics In Compan An Med. 27: 47-50.
Which one answer choice best completes the following statement? Viscoelastic tests (thromboelastography [TEG] and rotational thromboelastometry [ROTEM]) provide a better assessment of acute traumatic coagulopathy (ATC) compared to traditional PT and aPTT because,
a. ) Viscoelastic tests assess global coagulation affording analysis of coagulation, clot strength, and fibrinolysis whereas PT and aPTT do not assess beyond the initiation of coagulation.
b. ) Viscoelastic tests assess coagulation up to the fibrin clot whereas PT & aPTT assess coagulation from fibrin formation to fibrinolysis.
c. ) Viscoelastic tests are a subjective and objective analysis of clinical signs of ATC whereas PT & aPTT assess only fibrin formation.
a.) Viscoelastic tests assess global coagulation affording analysis of coagulation, clot strength, and fibrinolysis whereas PT and aPTT do not assess beyond the initiation of coagulation.
Palmer & Martin, JVECCS, Traumatic coagulopathy – Part 1: Pathophysiology and diagnosis. Pg. 70
Which one of the following answer pairs are considered the two main initiators of Acute Traumatic Coagulopathy?
a. Hemodilution & metabolic alkalosis
b. Metabolic acidosis & hyperthermia
c. Hyperthermia and neurohormonal mediators
d. Severity of tissue trauma & systemic hypoperfusion
d. Severity of tissue trauma & systemic hypoperfusion
Palmer & Martin, JVECCS, Traumatic coagulopathy – Part 1: Pathophysiology and diagnosis. Pg. 72
Choose the single correct answer:
a. Chediak – Higashi Syndrome is a rare disorder characterized by a failure of activation of β1 - , β2 - , and β3 – type integrins that also typically have high leukocyte counts and increased infection susceptibility.
b. Glanzmann thrombasthenia is a platelet disorder in which glycoprotein complex IIb – IIIa (fibrinogen receptor) is absent or reduced on the platelet surface causing abnormalities of clot retraction.
c. Kindlin – 3 Disorders are autosomal recessive genetic defects characterized by abnormal leukocyte, melanocyte, and platelet granulation.
b. Glanzmann thrombasthenia is a platelet disorder in which glycoprotein complex IIb – IIIa (fibrinogen receptor) is absent or reduced on the platelet surface causing abnormalities of clot retraction.
Boudreaux, JVECCS, Inherited platelet disorders, pgs. 4, 5, & 8
Which of the following inherited disorders causes abnormal clot retraction due to a dysfunctional GPIIb/IIIa complex?
A. Kindlin-3
B. Glanzmann’s thrombasthenia
C. Chediak-Higashi syndrome
D. CalDAG-GEFI mutation
B. Glanzmann’s thrombasthenia
Harvey, Ch. 7 Coagulation and Platelet Disorders, pg. 217
Which one of the following coagulation factor deficiencies may result in a prolonged APTT with normal PT?
A. Factor II
B. Factor VII
C. Factor VIII
D. Factor X
C. Factor VIII
Harvey, Ch. 7 Coagulation and Platelet Disorders, pg. 204-205
Anticoagulant rodenticides directly inhibit the enzyme ______________, preventing activation of the Vitamin K dependent coagulation factors ___, ___, ___ and ___.
A. Vitamin K carboxylase; II, VII, IX, X
B. Vitamin K carboxylase; VIII, IX, X, XI
C. Vitamin K epoxide reductase; II, VII, IX, X
D. Vitamin K epoxide reductase; VIII, IX, X, XI
C. Vitamin K epoxide reductase; II, VII, IX, X
Harvey, Ch. 7 Coagulation and Platelet Disorders, pg. 222
What coagulation factor does tissue factor typically form complexes with?
a. FVIII
b. FVI
c. FV
d. FIV
a. FVIII
Source: O’Brien, M.; The Reciprocal Relationship between Inflammation and Coagulation. 2012; Pg. 47.
Patients with hemophilia A usually have which of the following abnormalities on coagulation testing?
a. Increased PT and normal PTT
b. Increased PTT and normal PT
c. Normal PTT and normal PT
d. Increased PTT and increased PT
b. Increased PTT and normal PT
Source: Barr, T. and McMichael, M.; Inherited Disorders of Hemostasis in Dogs and Cats. 2012; Pg. 55.
A deficiency in which coagulation factor would cause an increased PTT and ACT but no clinical bleeding disorder?
a. FVII
b. FIX
c. FX
d. FXII
d. FXII
Source: Harvey’s Hematology Atlas - Ch. 7, Pg. 223.
Which one of the following is NOT a mechanism by which inflammatory mediators activate coagulation ?
a. Activation of protein C by binding thrombomodulin
b. Expression of tissue factor (TF) by stimulated monocytes
c. Release of phosphatidylserine-expressing microparticles
d. Release of von Willebrand factor by stimulated endothelial cells
a. Activation of protein C by binding thrombomodulin
O’Brien, M. The reciprocal relationship between inflammation and coagulation. Top Companion Anim Med. 2012 May ; 27(2):46-52. (p. 47, 49)
Which of these are currently the most sensitive laboratory tests for early diagnosis of disseminated intravascular coagulation in dogs ?
a. Thrombin-antithrombin complexes and hyperfibrinogenemia
b. Low antithrombin and increased fibrinolytic products
c. Prolonged partial thromboplastin time and thrombocytopenia
d. Prolonged prothrombin time and hypofibrinogenemia
b. Low antithrombin and increased fibrinolytic products
Stokol, T. Laboratory diagnosis of disseminated intravascular coagulation in dogs and cats : the past, the present and the future. Vet Clin North Am Small Anim Pract. 2012 Jan ; 42(1):189-202. (p. 195)
Which one of these test profiles is generally reported with rodenticide toxicity?
a. PT is prolonged and PTT remains normal
b. PT is prolonged earlier than PTT
c. PTT is prolonged earlier than PT
d. PT and PTT are prolonged simultaneously
b. PT is prolonged earlier than PTT
Veterinary Hematology : a Diagnostic Guide and Color Atlas, Chapter 7 : Evaluation of Hemostasis : Coagulation and Platelet Disorders, p. 222
What is an example of an extrinsic platelet disorder:
A. Glanzmann thrombasthenia B. Dense Granule Defect C. von Willebrand disease D. Chediak-Higashi Syndrome
C. von Willebrand disease
pg. 2, 4-5; Boudreaux MK. Inherited platelet disorders. JVECC 2012 1-12
Glanzmann thrombasthenia is characterized by the absence or reduction of:
A. von Willebrand factor B. dense granules C. ADP D. glycoprotein complex IIb-IIIa
D. glycoprotein complex IIb-IIIa
pg. 3-5; Boudreaux MK. Inherited platelet disorders. JVECC 2012 1-12
Which of the following are NOT part of Virchow’s triad, promoting thrombosis?
A. hypercoagulability B. hypervolemia C. endothelial injury D. turbulent blood flow
B. hypervolemia
pg 668-669; Schalm’s Veterinary Hematology,6th ed. Weiss & Wardrop, 2010
Which receptor does clopidogrel interact with to inhibit thrombosis?
a. Antagonist for ADP P2Y12 receptor
b. Agonist for the ADP P2Y12 receptor
c. Antagonist for integrin α2bβ3
d. Agonist for integrin α2bβ3
e. Inhibition of COX-1 which leads to decreased TxA2 production
a. Antagonist for ADP P2Y12 receptor
Page 52-54. C) is true for abciximab, tirofiban and eptifibatide.
Source: Source: Wiinberg, B., et al., Diagnosis and treatment of platelet hyperactivity in relation to thrombosis in dogs and cats. J Vet Emerg Crit Care (San Antonio), 2012. 22(1): p. 42-58.
Which of the following 3 phases of coagulation correctly lists the main coagulation factors involved?
a. Initiation: tissue factor on tissue factor bearing cell, F9 and complex of F8 and F10 which activates thrombin; amplification: non-activated platelet, F5, F11, F8 and vWF; propagation: activated platelet, F8, F5, F11, and complex of F8 and F10 that activates thrombin
b. Initiation: tissue factor on tissue factor bearing cell, F7 and complex of F5 and F8 which activates thrombin; amplification: non-activated platelet, F5, F11, F8 and vWF; propagation: activated platelet, F8, F9, F11, and complex of F5 and F8 that activates thrombin
c. Initiation: tissue factor on tissue factor bearing cell, F7 and complex of F5 and F10 which activates thrombin; amplification: non-activated platelet, F5, F11, F8 and vWF; propagation: activated platelet, F8, F9, F11, and complex of F5 and F10 that activates thrombin
d. Initiation: tissue factor on tissue factor bearing cell, F10 and complex of F5 and F7 which activates thrombin; amplification: non-activated platelet, F5, F11, F8 and vWF; propagation: activated platelet, F7, F8, F9, and complex of F5 and F7 that activates thrombin
c. Initiation: tissue factor on tissue factor bearing cell, F7 and complex of F5 and F10 which activates thrombin; amplification: non-activated platelet, F5, F11, F8 and vWF; propagation: activated platelet, F8, F9, F11, and complex of F5 and F10 that activates thrombin
Page 44.
Source: Wiinberg, B., et al., Diagnosis and treatment of platelet hyperactivity in relation to thrombosis in dogs and cats. J Vet Emerg Crit Care (San Antonio), 2012. 22(1): p. 42-58.
Under high shear conditions in the arteries, how do platelets bind to the endothelium?
a. Directly to exposed collagen via GP6 and GP1a2a
b. Indirectly binds to exposed collagen via GP-1b and vWF
c. Indirectly binds to exposed collagen via GP-2b3a and vWF
d. Indirectly binds to exposed collagen via GP-1b and thrombospondin-1
e. B and D
e. B and D
b. Indirectly binds to exposed collagen via GP-1b and vWF
d. Indirectly binds to exposed collagen via GP-1b and thrombospondin-1
Page 45 (Wiinberg) and page 195 (Harvey). A) this is true in low shear conditions (e.g. veins) c) GP2b/3a is essential for normal platelet aggregation Source: Harvey, JW: Veterinary Hematology: a Diagnostic Guide and Color Atlas, Saunders, 2012. Source: Wiinberg, B., et al., Diagnosis and treatment of platelet hyperactivity in relation to thrombosis in dogs and cats. J Vet Emerg Crit Care (San Antonio), 2012. 22(1): p. 42-58.
Resting platelets rely upon mediators for activation. Which one of the following is NOT an activator?
A. vWF
B. Collagen
C. Thrombin
D. Tissue Factor
D. Tissue Factor
Diagnosis and treatment of platelet hyperactivity in relation to thrombosis in dogs and cats, Journal of Veterinary Emergency and Critical Care 22(1) 2012, pg 45
The extrinsic coagulation cascade is activated when tissue factor binds to which circulating coagulation factor?
A. Factor V
B. Factor VII
C. Factor VIII
D. Factor X
B. Factor VII
Laboratory Diagnosis of Disseminated Intravascular Coagulation in Dogs and Cats: The Past, the Present, and the Future pg 190
Which of the following coagulation factors should NOT be affected by vitamin K deficiency?
A. Factor II
B. Factor V
C. Factor VII
D. Factor IX
B. Factor V
Harvey Evaluation of Hemostasis: Coagulation and Platelet Disorders pg 198
Which of the following is true regarding Hemophilia in dogs?
A. PT, PTT are both prolonged with Hemophilia A and Hemophilia B
B. Hemophilia B is the most common hereditory defect in dogs
C. Factor VIII deficiency characterizes Hemophilia A
D. Hemphophilia B is restricted to Shapr Pei dogs, German shepherds and DSH cats
C. Factor VIII deficiency characterizes Hemophilia A
hemostasis, Table 86.1
Which of the following is true regarding Fibrinogen deficiency?
A. Hereditary fibrinogen defects are more common than acquired defects. B. Hereditary fibrinogen defects are often associated with deficiencies of other factors. C. The half-life if fibrinogen is short compared to other factors and requires frequent transfusions. D. Cryoprecipitate is considered the treatment of choice for patients with fibronigen defects.
D. Cryoprecipitate is considered the treatment of choice for patients with fibronigen defects.
Hemostasis 664
Which of the following is true regarding Thrombin?
A. Thrombin generation reflects the final step in hemostasis.
B. Bound thrombin has a short half life compared to free thrombin.
C. Thrombin back activates several upstream cofactors and proteases
D. Thrombin’s role is limited to the secondary coagulation cascade.
C. Thrombin back activates several upstream cofactors and proteases
Chapter 84 649
