Hemostasis and Tests

Question 1

3 main stages of hemostasis

Answer 1

Primary (minutes, form platelet plug)
Secondary (hours, coagulation cascade to form fibrin net)
Fibrinolysis (days/weeks, activation of plasmin to break down fibrin clot)

Question 2

Steps in primary hemostasis

Answer 2

Vessel wall injury
Vasoconstriction
Turbulent blood flow
Circulating vWF binds to subendothelial collage
VWF binds platelet GP Ib receptor
Platelet aggregation via GPIIbIIIa receptors and fibrinogen
PLTs shape change to increase phospholipid SA
PLTs release granules

Question 3

Bleeding picture with primary hemostasis defects

Answer 3

Platelets or vWF
Excessive bruising
Mucosal bleeding (epistaxis, gum bleeds, GI bleeding, menorrhagia, post op)

Question 4

3 types of von Willebrand disease

Answer 4

Type 1: moderate deficiency
Type 2: does not work
Type 3: severe deficiency

Question 5

3 tests for VWF

Answer 5

VWF antigen (quantitative)
VWF activity (qualitative - tests GP1b binding)
Factor 8 activity (qualitative - similar to VWF Ag level)

Question 6

4 vitamin K dependent factors

Answer 6

10, 9, 7, 2

Question 7

1. 4 factors in the common pathway
2. 2 things in the extrinsic pathway
3. 4 factors in the intrinsic pathway

Answer 7

1. 1, 2, 5, 10
2. factor 7, tissue factor
3. 8, 9, 11, 12

Question 8

Bleeding picture with secondary hemostasis defects

Answer 8

Neonates: umbilical stump bleeding, ICH
Recurrent joint and/or IM bleeds
Delayed bleeding post op

Question 9

What factors are involved in hemophilia

1. A
2. B

Answer 9

1. Factor 8

2. Factor 9

Question 10

Which pathways are measured by

1. PTT
2. PT/INR

Answer 10

1. Intrinsic and common

2. Extrinsic and common

Question 11

Mixing studies

Answer 11

1:1 mix of patient and normal plasma, then repeat the PTT (or PT)
If clot time corrects = factor deficiency
If clot time does not correct = inhibitor present

Question 12

Protein C and Protein S

Answer 12

When activated they are natural inhibitors of coagulation
Vitamin K dependent
Inactivate key cofactors FV1 and FVIIIa

Question 13

Virchow’s triad

Answer 13

Endothelial injury
Stasis
Hypercoagulability

Question 14

Fibrinolysis

Answer 14

Tissue plasminogen activator (tPA) released by damaged endothelium
Converts plasminogen to plasmin
Plasmin chews up fibrin clot and makes D-dimer

Question 15

Tranexamic acid (TXA)

Answer 15

Antifibrinolytic drug

Very useful

Question 16

D-dimer

Answer 16

Reflects overall systemic clotting activity (production and lysis)