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Block 7 Week 4 > Fung: Coagulation > Flashcards

Fung: Coagulation Flashcards

1
Q

Disorders of hemostasis can be divided into what two types?

A

hemorrhagic disorders - excessive bleeding

thrombotic disorders - clot formation

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2
Q

Hemostasis is defined as the balance between what two factors?

A

clotting and thrombosis

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3
Q

Normal hemostasis occurs in these three steps

A
  1. vasoconstriction
  2. platelet aggregation
  3. fibrin formation
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4
Q

Reduces blood flow to the area
Mediated by reflex neurogenic mechanisms and augmented by local secretion of endothelin
Transient effect

A

vasconstriction

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5
Q

Platelets adhere to the endothelium and are activated

This process leads to aggregation and the beginnings of a clot

A

primary hemostasis

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6
Q

Tissue factor is exposed at the site of vascular injury

Sets in motion a cascade of reactions that leads to thrombin formation

A

secondary hemostasis

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7
Q

3 layers of the blood vessel

A

intima
media
adventitia

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8
Q

The intima contains (blank)
The media is a layer of (blank)
The adventitia is rich in (blank)

A

endothelium
smooth muscle
connective tissue

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9
Q

How does the vascular endothelium actively regulate hemostasis?

A

inhibits platelets
suppresses coagulation
promotes fibrinolysis
modulates vascular tone and permeability

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10
Q

Upon vascular injury, what is exposed? What is released?

A

tissue factor is released; collagen and vWF are exposed

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11
Q

What two layers of the blood vessel mediate vasoconstriction?

A

media and adventitia

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12
Q

Describe the process of primary hemostasis

A

Vascular damage leads to ezposure of collagen and vWF; platelets adhere, and change shape; platelets release granules containing ADP and TXA2, which recruit additional platelets to the site of injury; aggregation occurs and creates a hemostatic plug

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13
Q

Platelets are derived from (blank) maturation

A

megakaryocyte

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14
Q

This component of the platelet cytoskeleton bind vWF

A

GP Ib/V/IX

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15
Q

This component of the platelet cytoskeleton binds fibrinogen and causes platelets to bind together

A

GP IIb/IIIa

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16
Q

This component of the platelet cytoskeleton initiates platelet activation when bound by ADP

A

ADP receptor

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17
Q

Which are more numerous in platelets, alpha or dense granules?

A

alpha

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18
Q

What are the contents of alpha granules?

A

vWF
fibrinogen
factor V, FXI

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19
Q

What are the contents of dense granules?

A

ATP
ADP
calcium
serotonin

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20
Q

What do platelets bind to at the site of endothelial injury?

A

exposed collagen and vWF

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21
Q

Platelet adhesion is mediated by (blank) binding to vWF on the endothelium.

A

GP Ib/V/IX

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22
Q

What does platelet activation lead to?

A

shape change
release of alpha and dense granules
initiation of thromboxane A2 pathway
GP IIb/IIIa changes to its active form to cause platelets to adhere to one another

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23
Q

Explain what happens in secondary hemostasis

A

tissue factor is released
phospholipid complexes are expressed
thrombin is activated
fibrin polymerizes (cross-links)

24
Q

In the extrinsic pathway, (blank) released w endothelial injury. It is cleaves factor (blank) into factor (blank). Factor (blank) can then act on factor (blank) to make it (blank). 10a then converts prothrombin into (blank). Thrombin converts (blank) to fibrin and allows for cross linking of fibrin.

A

tissue factor; 7; 7a; 7a; 10; 10a; thrombin; fibrinogen

25
Q

The intrinsic pathway starts with factor (blank) converting to factor (blank). Factor (blank) is then converted to (blank), and (blank) to (blank). Then, this enters the common pathway causing Factor 10 to convert to 10a, which makes prothrombin convert to thrombin. Thrombin acts of fibrinogen to form fibrin, which ultimately gets cross-linked.

A

12; 12a; 11; 11a; 9; 9a

26
Q

Both of these factors convert prothrombin to thrombin.

A

5a and 10a

27
Q

Most of the factors in the coagulation cascade are produced in the (blank) except for von Willebrand factor which is produced in the (blank) and (blank)

A

liver; endothelial cells; megakaryocytes

28
Q

Summary of coag:
Defect in the vessel wall exposes (blank)
Circulating platelets bind to (blank) and undergo shape change
(blank) allows for aggregation of activated platelets
Aggregated platelets degranulate and activate (blank) which recruits more platelets
Activation of extrinsic and intrinsic pathways eventually converts fibrinogen to (blank)

A 
collagen and vWF;
GPIb;
GPIIbIIIa/fibrinogen; 
thromboxane A2;
fibrin
29
Q

These factors inhibit thrombin

A 
thrombin
FIXa
FXa
FXIa
FXIIa
30
Q

These factors inhibit activated C protein

A

FVa

FVIIIa

31
Q

Tissue factor pathway inhibitor/extrinsic pathway inhibitor

A

tissue factor-FVIIa-FXa

32
Q

This degrades fibrin

A

plasmin

33
Q

Two ways to evaluate hemostasis

A

platelets (platelet count, bleeding time, platelet function, platelet flow cytometry)
coagulation (alpha-PTT, PT, thrombin time)

34
Q

Used to screen for qualitative platelet disorders or von Willebrand disease
Not a useful test for predicting the risk of bleeding during surgery
Should not be used in patients without a history of excessive bleeding
Normal range is 1.5-9.5 minutes

A

bleeding time

35
Q

When is bleeding time prolonged?

A 
von Willebrand disease
inherited platelet disorders
uremia
aspirin ingestion
low platelet count
36
Q

In vitro evaluation of platelet aggregation

Performed on platelet-rich plasma that is exposed to various agonists

A

Platelet aggregometry

37
Q

What are some agonists that you would expose platelet-rich plasma to to see if aggregation occurs?

A 
ADP
epi
arachidonate
collagen
ristocetin
38
Q

What is platelet flow cytometry used to diagnose?

A

deficiencies of platelet surface glycoproteins

disorders of platelet activation

39
Q

Detects cell surface proteins with fluorescently labeled antibodies

A

platelet flow cytometry

40
Q

What is platelet count? What is the normal range for platelets?

A

actual platelet count determined on automated counters; reference = 140-400,000 cells/mL

41
Q

Which pathways does the prothrombin time evaluate?

A

extrinsic and common pathways

42
Q

When measuring prothrombin time, what is added to plasma to measure the time to clot?

A

tissue factor and thromboplastin with excess Ca++

43
Q

If prothrombin time is prolonged, what factors might be deficient or inhibited?

A

factor 7, 10, 5, 2, fibrinogen

44
Q

Prothrombin time is used to monitor (blank) therapy

A

warfarin (coumadin)

**warfarin is an anti-coagulant

45
Q

Used to reduce interlaboratory variation that results from differing thromboplastin sensitivities to coumadin

A

INR (international normalized ratio)

46
Q

What pathways can the activated partial thromboplastin time (alphaPTT) be used to evaluate?

A

intrinsic and common pathways

47
Q

When measuring activated partial thromboplastin time, what is added to plasma to measure the time to clot?

A

phospholipid is added to the plasma with excess Ca++

48
Q

If the activated partial thromboplastin time is prolonged, what might this indicate a deficiency in?

A

any of the factors in the common or intrinsic pathways (12, 11, 9, 8, 5, 10, 2, fibrinogen)

49
Q

Used to monitor heparin, hirudin or argatroban therapy

A

activated partial thromboplastin time

50
Q

What is the thrombin time used to test for?

A

the presence of functional fibrinogen

51
Q

What are mixing studies used to determine?

A

the cause of prolonged clotting times

to screen for the presence of inhibitors

52
Q

Describe a mixing study. How can you tell if the clotting problem is due to a factor deficiency or the presence of an inhibitor?

A

mix the patient’s plasma with normal test plasma (normal clotting factors); if there is at least 50% activity, the problem was due to a factor deficiency; if there is less than 50% activity, there is an inhibitor present

53
Q

When are D-dimers formed?

What does their presence indicate?

A

when fibrin is degraded by plasmin; indicate that fibrin has been formed and degraded

54
Q

Version of platelet aggregation where patient plasma is added to formalin-fixed normal platelets in the presence of ristocetin
Normal patients will have platelet agglutination
vWF deficient patients will have decreased aggregation

A

von Willebrand factor assay

55
Q

This is another name for von Willebrand factor

A

Ristocetin

56
Q

T/F: You can perform individual factor assays to show a specific factor deficiency

A

True

Block 7 Week 4 (8 decks)

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