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?

A

PT

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
Q

What is a mixing study?

A

mix normal plasma with patient plasma

26
Q

What would the mixing study look like for hemophilia A?

A

can regain coagulation

27
Q

What does mixing study look like for coag factor inhibitor?

A

FAILS, antibody will hit normal plasma too and it won’t bind (cannot correct PTT)

28
Q

What is Von Willebrand’s Disease?

A

defect in VWF (MOST COMMON INHERITED COAG DISORDER)

autosomal dominant

29
Q

What do lab findings look like for VWF disease?

A

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
Q

What is the treatment of VWF disease?

A

desmopressin (increases release of VWF from Weibel-Palade bodies of endothelial cells)

31
Q

What does vitamin K deficiency result in?

A

disrupts function of multiple coag factors

vit K is essential for gamma carboxylating factors

32
Q

How does coumadin work?

A

blockes epoxide reductase

33
Q

Who is prone to vitamin K deficiency?

A

1) newborns
2) long term antibiotic therapy
3) malabsorption

34
Q

What are 3 reasons why liver failure can lead to bleeding problems?

A

1) decreased production of coag factors

2) decreased activation of vitamin K by epoxide reductase

35
Q

Why can large volume transfusions lead to bleeding problems?

A

dilutes coag factors (relative deficiency)