Primary Hemostasis

Question 1

Hemostasis

Answer 1

-the stoppage of bleeding
-Balance between
>form clots when needed; prevent clot formation when not needed

Question 2

What affects hemostasis?

Answer 2

-depends on integrity of blood vessels, platelet numbers and function and status/balance of coagulation factors and their inhibitors

Question 3

Coagulopathy

Answer 3

-a disruption in the ability to form a clot

Question 4

Hemostatic disorder

Answer 4

-a disruption that leads to insufficient clot formation OR excessive clot formation
>can be related to hemorrhage

Question 5

Virchow’s Triad

Answer 5

**all contribute to thrombosis (predisposition for clots which clog body)
-Hypercoagulable state- hyperactive platelets and procoagulation enzymes
-Abnormal Blood flow- hyperviscosity, narrowing of vessels
-Endothelial damage

Question 6

Timing of primary and secondary hemostasis

Answer 6

-occur at the same time, but both have a different story

Question 7

Phases of primary hemostasis

Answer 7

**looking at platelet numbers and platelet function
-Vascular phase
-Platelet phase

Question 8

Vascular phase of primary hemostasis

Answer 8

-Reflex vasoconstriction immediately which results in slower blood flow allowing the platelets time and exposure to subendothelial collagen under the damaged endothelial cells
>also contributes with platelets being pushed up against the walls, increasing their chances of contacting damaged wall
-Tissue factor is released by the subendothelial adventitial cells which stimulates secondary hemostasis

Question 9

Platelet phase of primary hemostasis

Answer 9

-Platelets congregate around exposed collagen
>adhesion, aggregation and shape change from discoid to spherical
>P-selectin will enhance platelet rolling along endothelial cells adjacent to damaged focus
-clot retraction can also occur and helps reduce size of area that needs to be repaired

Question 10

GpIb

Answer 10

-used for platelet anchoring to underlying collagen via the vWF

Question 11

vWF

Answer 11

-von Willebrand factor
-released by damaged endothelial cells
-mediates binding of collagen to GpIb

Question 12

GpIb and vWF main purpose

Answer 12

-binding platelets to collagen

Question 13

GpIIbIIIa

Answer 13

-Binds fibrinogen and enhances platelet-platelet cohesion
>platelets will grab fibrinogen and different platelets will fight over it. These results in better binding between the platelets

Question 14

P-selectin

Answer 14

-not exclusive to platelets
-enhances platelet rolling along endothelial cells adjacent to damaged focus

Question 15

Platelet adhesion within primary hemostasis (platelet phase)

Answer 15

-takes seconds
-platelets have smaller number of surface glycoprotein called GpIb. The GpIb will bind to the vWF and only the vWF that is trapped within the extracellular collagen will bind it, which leads to the anchoring of platelet to exposed collagen

Question 16

Platelet activation

Answer 16

-When platelets bind to collagen and substances such as thrombin, it leads to the calcium release within the cell which triggers cell changes
-An activated platelet will have a major shape change, increased GpIb presence on surface, and increased expression of GpIIbIIIa on surface to bind fibrinogen

Question 17

Phospholipase activation

Answer 17

-occurs during platelet activation
-leads to Thromboxane A2 which further promotes aggregation and vasoconstriction

Question 18

Platelet secretion

Answer 18

-platelets degranulate, releasing contents of alpha granules (promoting coagulation) and dense granules (promote aggregation of platelets and coagulation; contain Ca2+)

Question 19

Platelet plug

Answer 19

-provide initial physical plug to stop hemorrhage, but also help retract the clot and make the repair area smaller
-important for secondary hemostasis

Question 20

Platelet activation charge change

Answer 20

-When platelets activated, they change shape from discoid to spherical, but also the negatively charged phosphatidylserine moves from inside the cell membrane to the outside where it is exposed. Negative change will bind Ca which is important for secondary hemostasis

Question 21

Inhibit procoagulation

Answer 21

-the upstream and downstream healthy endothelial cells will increase substance production when they sense damaged endothelium nearby. This is a way to prevent coagulation at the healthy sites.
>produce PGI2 which inhibits platelet aggregation

Question 22

Platelet aggregation

Answer 22

-takes minutes (aspirin prevents the thromboxane production and therefore aggregation)
-requires fibrinogen and Ca
-increased expression of GpIIbIIIa on platelet surface promotes platelet binding between platelets as receptors bind circulating fibrinogen

Question 23

Von Willebrand disease

Answer 23

-not producing vWF or in type 2 they produce it but it is not properly functioning; means they won’t stick to collagen and then platelets cannot grab the collagen/vWF complex for clotting

Question 24

Clinical manifestations of von Willebrand disease

Answer 24

-Petechiation
-Purpura

Question 25

vWF ELISA test

Answer 25

-testing for how much vWF present in patient
-70-120% is normal
-40-70% questionable
-Less than 40%- likely have Type I

Question 26

Type II vWD detection

Answer 26

-must use multimeric analysis to determine whether multimers are present

Question 27

Type III vWD

Answer 27

-very rare, typically patients die in utero

Question 28

Thrombocytopenia

Answer 28

-defect in platelet function, but hemorrhage may not occur depending on platelet count
-detect by CBC or smear evaluation
-mainly acquired but can be inherited
-normal in Cavalier King Charles Spaniel

Question 29

Acquired thrombocytopenia?

Answer 29

Mainly acquired
>increased utilization (ex. DIC, vasculitis, etc.)
>reduced production (ex.marrow disease)
>Destruction (ex. immune mediated thrombocytopenia)
>Sequestration (typically mild)
>Secondary to hemorrhage (typically mild)

Question 30

Inherited thrombocytopathia

Answer 30

1.vWD- platelets GpIb cannot attach to collagen
2.Bernard-Soulier syndrome (GpIb deficiency) – no GpIb to attach to VWF, so platelets can’t stick/clot

Question 31

Thrombopathia

Answer 31

-normal platelet count, through platelet function or platelet-associated factors are abnormal