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)