GMS6530 Blood Exam Questions And Correct Answers Graded A+
Latest Update 100% Pass Guaranteed
Overview of Haemostasis
1. vascular phase = vasoconstriction (the diameter of the blood vessel is reduced and
therefore less blood flows into the area)
2. platelet phase = plug formation-the platelets become sticky and attach to collagen in
the damaged vessel wall and then to each other in a process called aggregation
3. plasmatic phase = fibrin clot formation coagulation cascade-the coagulation cascade
results in the activation of thrombin which in turn converts fibrinogen into fibrin
4. fibrinolytic phase = plasmin degrades fibrin (dissolves the clot)
platelet aggregation overview
tissue injury (exposed collagen) --> platelet recruitment to collagen [via vWF]--> platelet
degranulation --> ADP + 5-HT + TxA2--> GPIIb/IIIa receptor activation--> platelet
aggregation
coagulation cascade
-composed of clotting factors arranged in two pathways
-intrinsic and extrinsic systems
extrinsic system
-activated as a result of tissue injury and collagen exposure
-occurs during the injury of tissue
-skip several steps
-in seconds
-7
intrinsic pathway
-contact with surface
-almost all of the pathways are required
-relatively slow
,-12,11,9,8
T/F: thrombin, the final enzyme, converts soluble fibrinogen to insoluble fibrin mesh in
which blood cells become trapped, thus forming the clot; this constitutes the common
pathway
True
vitamin k dependent clotting factors
II, VII, IX, X,------ (2,7,9,10)
regulation of coagulation
-antithrombin III directly inhibits activated factor 10 and activated factor 2 (thrombin)
fibrinolytic system
-dissolves small, inappropriate clots; it also dissolves clots at a site of damage once the
damage is repaired
-plasminogen gets converted to plasmin
-plasmin cleaves polymerized fibrin to dissolve blood clot
standard laboratory tests
-aPTT- activated Partial Thrombopastin Time
-PT- Prothrombin time
-Bleeding time
-Platelet count
aPTT
-activated partial thromboplastin time
-measure of the intrinsic pathway
-normal range 25-35 seconds
PT
-prothrombin time
-measure of the extrinsic pathway and common pathway
-normal range 11-15 seconds
-variability between laboratories- INR (international normalized ratio = 1.0)
, Bleeding time
-platelet-blood vessel interaction abnormality
-normal range 1-6 minutes
platelet count
-normal range 150,000-400,000/ microliter
anticoagulants to know
-Heparin
-low molecular weight heparins (LMWH)
-warfarin
-direct thrombin inhibitors
-direct factor Xa inhibitors (-xa-bans)
fibrinolytics to know
-alteplase
-streptokinase
antiplatelet agents to know
-aspirin
-ticlopidine
-clopidogrel
-prasugrel
the ideal anticoagulant
-prevents pathologic thrombosis and limits reperfusion injury
-allows a normal response to vascular injury and limit bleeding
-theoretically, would preserve TF/VIIa initiation in response to injury and attenuate
intrinsic pathway of clot propagation
-currently, such drug does not exist
-all existing anticoagulants and fibrinolytics have an increased bleeding risk as their
toxicity
heparin and low molecular weight heparins
Latest Update 100% Pass Guaranteed
Overview of Haemostasis
1. vascular phase = vasoconstriction (the diameter of the blood vessel is reduced and
therefore less blood flows into the area)
2. platelet phase = plug formation-the platelets become sticky and attach to collagen in
the damaged vessel wall and then to each other in a process called aggregation
3. plasmatic phase = fibrin clot formation coagulation cascade-the coagulation cascade
results in the activation of thrombin which in turn converts fibrinogen into fibrin
4. fibrinolytic phase = plasmin degrades fibrin (dissolves the clot)
platelet aggregation overview
tissue injury (exposed collagen) --> platelet recruitment to collagen [via vWF]--> platelet
degranulation --> ADP + 5-HT + TxA2--> GPIIb/IIIa receptor activation--> platelet
aggregation
coagulation cascade
-composed of clotting factors arranged in two pathways
-intrinsic and extrinsic systems
extrinsic system
-activated as a result of tissue injury and collagen exposure
-occurs during the injury of tissue
-skip several steps
-in seconds
-7
intrinsic pathway
-contact with surface
-almost all of the pathways are required
-relatively slow
,-12,11,9,8
T/F: thrombin, the final enzyme, converts soluble fibrinogen to insoluble fibrin mesh in
which blood cells become trapped, thus forming the clot; this constitutes the common
pathway
True
vitamin k dependent clotting factors
II, VII, IX, X,------ (2,7,9,10)
regulation of coagulation
-antithrombin III directly inhibits activated factor 10 and activated factor 2 (thrombin)
fibrinolytic system
-dissolves small, inappropriate clots; it also dissolves clots at a site of damage once the
damage is repaired
-plasminogen gets converted to plasmin
-plasmin cleaves polymerized fibrin to dissolve blood clot
standard laboratory tests
-aPTT- activated Partial Thrombopastin Time
-PT- Prothrombin time
-Bleeding time
-Platelet count
aPTT
-activated partial thromboplastin time
-measure of the intrinsic pathway
-normal range 25-35 seconds
PT
-prothrombin time
-measure of the extrinsic pathway and common pathway
-normal range 11-15 seconds
-variability between laboratories- INR (international normalized ratio = 1.0)
, Bleeding time
-platelet-blood vessel interaction abnormality
-normal range 1-6 minutes
platelet count
-normal range 150,000-400,000/ microliter
anticoagulants to know
-Heparin
-low molecular weight heparins (LMWH)
-warfarin
-direct thrombin inhibitors
-direct factor Xa inhibitors (-xa-bans)
fibrinolytics to know
-alteplase
-streptokinase
antiplatelet agents to know
-aspirin
-ticlopidine
-clopidogrel
-prasugrel
the ideal anticoagulant
-prevents pathologic thrombosis and limits reperfusion injury
-allows a normal response to vascular injury and limit bleeding
-theoretically, would preserve TF/VIIa initiation in response to injury and attenuate
intrinsic pathway of clot propagation
-currently, such drug does not exist
-all existing anticoagulants and fibrinolytics have an increased bleeding risk as their
toxicity
heparin and low molecular weight heparins