Secondary Hemostasis Flashcards

1
Q

_______ binds the platelet to VWF while _________ binds platelets to platelets (allowing aggregation)

A

Gp1b

GpIIb/IIIa

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2
Q

What is the end product of the coagulation cascade

A

thrombin

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3
Q

what does thrombin do?

A

convert fibrinogen to fibrin

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4
Q

What does fibrin do?

A

stabilize

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5
Q

Where are the factors of the coagulation cascade produced?

A

the liver

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6
Q

What 3 things do coagulation factors require for activation?

A

1) exposure to activating substance
2) phopholipid surface
3) calcium (derived from platelets)

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7
Q

What is the cause of secondary hemostasis?

A

factor abnormalities

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8
Q

What are the clinical features of secondary hemostasis disorders?

A

deep bleeding (into muscles and joints)

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9
Q

What does PT measure?

A

extrinsic and common pathway

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10
Q

What does PTT measure?

A

intrinsic and common pathways

intrinsic has more factors involved, measured by the test with more letters

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11
Q

The goal of the coagulation cascade is to produce __________

A

factor 10 (the perfect 10)

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12
Q

What activates factor 12?

A

subendothelial collagen

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13
Q

What activates factor 7?

A

tissue thromboplastin

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14
Q

What initiates the extrinsic pathway?

A

factor 7

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15
Q

What test is a better measurement for the heparin effect?

A

PTT

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16
Q

What test is a better measurement for coumadin effect?

17
Q

What is the cause of hemophilia A?

A

genetic deficiency in factor 8 (aaaaate)

X-linked recessive (can get de novo mutations)

18
Q

What are the signs and symptoms of patients with disorders of secondary hemostasis?

A

deep tissue, joint, and postsurgical bleeding

19
Q

What are the lab findings for disorders of secondary hemostasis?

A

1) HIGH PTT, normal PT
2) LOW factor 8
3) normal platelet count and bleeding time

20
Q

What is the treatment for hemophilia A?

A

recombinant factor 8

21
Q

What is the cause of hemophilia B?

A

factor 9 deficiency

22
Q

How does hemophilia B look clinically?

A

the same as A! (both affect intrinsic pathway)

23
Q

What is the most common coag factor inhibitor?

A

anti-factor 8

resembles hemophila A

24
Q

how do you determine the difference between hemophilia A or coag factor inhibitor disease?

A

mixing study

25
What is a mixing study?
mix normal plasma with patient plasma
26
What would the mixing study look like for hemophilia A?
can regain coagulation
27
What does mixing study look like for coag factor inhibitor?
FAILS, antibody will hit normal plasma too and it won't bind (cannot correct PTT)
28
What is Von Willebrand's Disease?
defect in VWF (MOST COMMON INHERITED COAG DISORDER) autosomal dominant
29
What do lab findings look like for VWF disease?
1) HIGH bleeding time 2) HIGH PTT, normal PT 3) abnormal ristocetin test lack of stability of factor 8 to change the labs but NOT to create clinical problems
30
What is the treatment of VWF disease?
desmopressin (increases release of VWF from Weibel-Palade bodies of endothelial cells)
31
What does vitamin K deficiency result in?
disrupts function of multiple coag factors vit K is essential for gamma carboxylating factors
32
How does coumadin work?
blockes epoxide reductase
33
Who is prone to vitamin K deficiency?
1) newborns 2) long term antibiotic therapy 3) malabsorption
34
What are 3 reasons why liver failure can lead to bleeding problems?
1) decreased production of coag factors | 2) decreased activation of vitamin K by epoxide reductase
35
Why can large volume transfusions lead to bleeding problems?
dilutes coag factors (relative deficiency)