GMS6530: BLOOD EXAM QUESTIONS AND
ANSWERS
Haemostasis overview
1. vascular phase = vasoconstriction (reduces blood flow)
2. platelet phase = plug formation (platelets adhere to collagen and aggregate)
3. plasmatic phase = fibrin clot formation coagulation cascade (activation of thrombin
that converts fibrinogen into fibrin)
4. fibrinolytic phase = plasmin degrades fibrin (dissolves the clot)
overview of platelet aggregation
tissue damage (exposed collagen) --> platelet recruitment to collagen (via vWF)-->
platelet degranulation --> ADP + 5-HT + TxA2--> GPIIb/IIIa receptor activation-->
platelet aggregation
coagulation cascade
-consists of clotting factors organized in two pathways
-intrinsic and extrinsic systems
extrinsic system
-tissue damage and exposure of collagen leads to activation
-operates during tissue injury
-bypasses several steps
-occurs in seconds
-7
intrinsic pathway
-surface contact
-requires almost all of the pathways
-relatively slow
-12,11,9,8
T/F: thrombin, the last enzyme, converts soluble fibrinogen to insoluble fibrin
mesh in which blood cells are trapped, forming the clot; this is 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
-activates antithrombin III in the plasma
-antithrombin inhibits thrombin (IIa), IXa, Xa
-not effective orally so given s.c or i.v
-has a rapid onset of action when given parenterally
-structure is a sulfated glycosaminoglycan
clinical of use of heparin
-used for immediate coagulation (example: therapy in myocardial infarction
-other uses are venous thrombosis, pulmonary embolism, and thrombosis prophylaxis
-used for 7-10 days followed by warfarin with a 3-5 day overlap
ANSWERS
Haemostasis overview
1. vascular phase = vasoconstriction (reduces blood flow)
2. platelet phase = plug formation (platelets adhere to collagen and aggregate)
3. plasmatic phase = fibrin clot formation coagulation cascade (activation of thrombin
that converts fibrinogen into fibrin)
4. fibrinolytic phase = plasmin degrades fibrin (dissolves the clot)
overview of platelet aggregation
tissue damage (exposed collagen) --> platelet recruitment to collagen (via vWF)-->
platelet degranulation --> ADP + 5-HT + TxA2--> GPIIb/IIIa receptor activation-->
platelet aggregation
coagulation cascade
-consists of clotting factors organized in two pathways
-intrinsic and extrinsic systems
extrinsic system
-tissue damage and exposure of collagen leads to activation
-operates during tissue injury
-bypasses several steps
-occurs in seconds
-7
intrinsic pathway
-surface contact
-requires almost all of the pathways
-relatively slow
-12,11,9,8
T/F: thrombin, the last enzyme, converts soluble fibrinogen to insoluble fibrin
mesh in which blood cells are trapped, forming the clot; this is 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
-activates antithrombin III in the plasma
-antithrombin inhibits thrombin (IIa), IXa, Xa
-not effective orally so given s.c or i.v
-has a rapid onset of action when given parenterally
-structure is a sulfated glycosaminoglycan
clinical of use of heparin
-used for immediate coagulation (example: therapy in myocardial infarction
-other uses are venous thrombosis, pulmonary embolism, and thrombosis prophylaxis
-used for 7-10 days followed by warfarin with a 3-5 day overlap
