Hematology

Question 1

tunica intima layer

Answer 1

barrier of endothelial cells in the vasculature; produces procoagulants and anticoagulants mediators, and fibrinolytic

Question 2

procoagulant mediators

Answer 2

von willebrand factor,
tissue factor (TF),
thromboxane A2 and Adenosine diphosphate (ADP),
collagen,
fibronectin

Question 3

anticoagulant mediators

Answer 3

nitric oxide (NO),
prostacyclin,
prostaglandin I2

Question 4

von Willebrand factor (vWF)

Answer 4

cofactor for coagulation cascade

Question 5

tissue factor (TF)

Answer 5

activates clotting cascade pathway during vessel injury

Question 6

thromboxane A2 and adenosine diphosphate (ADP)

Answer 6

vasoconstriction

Question 7

collagen

Answer 7

stimulates platelet attachment to the injured vessel wall

Question 8

fibronectin

Answer 8

facilitates anchoring of fibrin during the formation of a hemostatic plug

Question 9

nitric oxide (NO)

Answer 9

inhibits platelet adhesion and aggregation;
promotes vasodilation (smooth muscle relaxation)

Question 10

prostacyclin

Answer 10

causes vasodilation and interferes with platelet formation and aggregation

Question 11

prostaglandin I2

Answer 11

inhibits platelets

Question 12

Primary hemostasis (platelet plug)

Answer 12

no injury - nitric oxide and prostaglandin I2 releases which inhibit platelets

INJURY - thromboxane A2 releases which causes vasoconstriction; platelet plug is formed through adhesion, activation, and aggregation of platelets

Question 13

Adhesion (primary hemostasis)

Answer 13

1. collagen exposed
2. vonWillebrand factor released and binds to Gplb receptors on the platelet which anchors the platelets of the sub endothelium
3. platelets bind to the collagen and are activated

Note:
1. desmopressin causes the body to release more vWF
2. FFP and Cryo also help with this step bc they contain vWF and Factor 8

Question 14

Activation (primary hemostasis)

Answer 14

1. platelets are activated by binding to collagen
2. the platelets then release thromboxane A2 and ADP which activates other platelets and help with aggregation by allowing glycoproteins on platelets to bind to fibrinogen.
3. activated platelets will release contents from inside them such as fibrinogen, fibronectin, and vWF.

Question 15

aggregation (primary hemostasis)

Answer 15

1. activated platelets have 2 glycoproteins on their surface - Gp IIIa and Gp IIb
   together they help aggregate platelets to form a “plug”

Question 16

Secondary hemostasis / Coagulation Cascade

Answer 16

Intrinsic Pathway - begins with damage inside the vessel

extrinsic pathway - begins with damage outside the vessel

once either of these get to factor 10, the common pathway is initiated

eventually leading to formation of fibrinogen

Question 17

Intrinsic pathway

Answer 17

damage inside the vessel
blocked by heparin
diagnostic is apTT and ACT
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factor 12 (hageman) activated from collagen

activates factor 11 (plasma thromboplastin antecedent)

activated factor 9 (christmas) in presence of 4 (calcium)

factor 8 (anti hemophilic) is combined

which activates 10 (stuart-prower)
____________________________________
Note:
heparin blocks the Intrinsic pathway by 1. binding to antithrombin to block thrombin and 2. makes antithrombin work much better to block factors 2 and 9-12
protamine is the heparin reversal

Question 18

extrinsic pathway

Answer 18

initiated outside the vessel
blocked by warfarin
diagnostic is PT/INR
_____________________________
factor 3 (tissue factor) activated

activates factor 7 (stable)

which when activated 7 binds to factor 4 (calcium)

which activates 10 (stuart-prower)
___________________________________

Note:
warfarin blocks the extrinsic pathway bc it inhibits vit K from becoming active which in turn prevents 2, 7, 9, and 10

PT/INR measures warfarin effectiveness
12-14 sec Normal
x2 or 3 for warfarin

vit K and FFP are reversals of warfarin