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Fundamentals 2 > Hemostasis and Thrombosis > Flashcards

Hemostasis and Thrombosis Flashcards

1
Q

ecchymoses

A

larger bruises that color change as hemoglobin is broken down

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2
Q

petechiae

A

tiny hemorrhages

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3
Q

purpura

A

medium hemorrhages

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4
Q

hematoma

A

accumulation of blood in a tissue

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5
Q

hemarthrosis

A

hemorrhage into a joint

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6
Q

hemostasis by definition

A

stopping the flow of blood

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7
Q

3 stages of hemostasis

A

1) reflex vasoconstriction
2) primary hemostasis
3) secondary hemostasis

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8
Q

reflex vasoconstriction

A

baroreceptors detect low BP and vessels automatically constrict to roughly stop bleeding / increase BP

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9
Q

7 steps of primary hemostasis in general

A

1) endothelial injury
2) exposure of subendothelial vWF + collagen
3) platelet adhesion to vWF
4) change in platelet shape + receptor affinity change
5) secretion of granule contents
6) platelet recruitment and aggregation
7) platelet plug

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10
Q

what is primary hemostasis?

A

platelet plug

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11
Q

How do platelets adhere to vWF?

A

through Gp1B receptors

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12
Q

What does a change in platelet shape change affinity for?

A

GpIIb / II a affinity

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13
Q

What are platelets derived from?

A

megakaryocytes

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14
Q

what 3 receptors do platelets express? What are they for?

A

1) fibrinogen - GpIIb/a
2) vWF - Gp1B
3) collagen - a2B1

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15
Q

What do activated platelets express at their surface?

A

phosphatidylserine

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16
Q

how can you assess platelet function?

A

measure closure time

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17
Q

closure time

A

time it takes for blood to plug a small hole

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18
Q

what type of granules do platelets contain?

A

alpha and dense-core granules

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19
Q

What molecules is an activator of platelets?

A

ADP

*induces conformation change

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20
Q

Thromboxane A2

A

potent vasoconstrictor that promotes platelet aggregation and activation

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21
Q

How does aspirin work

A

inhibits COX

by inhibiting COX, you have less thromboxane A2 and less platelet activation

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22
Q

COX

A

normally catalyzes production of thromboxane A2

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23
Q

Plasminogen activator inhibitor (PAI)

A

secreted by endothelial cells

limits fibrinolysis and favors thrombosis

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24
Q

vWF

A

large protein in subendothelial tissue that allows platelets to bind

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25
Q

What links primary and secondary hemostasis?

A

vWF allows platelets to bind

vWF also stabilizes Factor VIII

26
Q

What is the end product of secondary hemostasis?

A

fibrin clot

27
Q

What is the first step of secondary hemostasis?

A

vascular injury expresses Tissue Factor which binds to and activates factor VII

28
Q

tissue factor

A

activates factor VII

membrane protein that is synthesized by “activated” endothelial cells, fibroblasts, and smooth muscle cells

29
Q

What are the coagulation factors?

A

a series of serine proteinases

30
Q

What does thrombin do?

A

converts fibrinogen to fibrin

triggers positive feedback

31
Q

What blood test measures the extrinsic pathway and common pathway?

A

PT

32
Q

What blood test measures the intrinsic pathway and common pathway?

A

PTT

33
Q

What does a long PT or PTT indicate?

A

clotting problem

takes too long to clot

34
Q

INR

A

compares PT to standard

35
Q

High INR indicates …

A

high likelihood of bleeding

36
Q

What is hemophilia associated with?

A

absence of factor VII

37
Q

After tissue factor activates, factor VII what happens?

A

factor IX is activated

38
Q

What factors does thrombin activate as part of positive feedback loop

A

factor 13, 11, 8 and 5

39
Q

Factor XIII

A

stabilizes fibrin clot by cross-linking fibrin

important for clot stabilization

40
Q

What can elevated D-Dimer indicate?

A

you had or have a clot somewhere that is currently being degraded

41
Q

Problems with D-dimer

A

use when suspicion is low/moderate as a screening test

not the best test

42
Q

How does D-dimer arise physiologically?

A

plasmin degrades the fibrin clot into D-dimers

43
Q

t-PA

A

converts plasimonogen to plasmin

*plasmin breaks down fibrin

44
Q

alpha2-antiplasmin

A

prevents plasmin by sequestering it

allows the clot to remain for longer

45
Q

what occurs at the same time as activation of the coagulation cascade?

A

fibrinolytic cascade is also set in motion

46
Q

urokinase

A

also converts plasminogen to plasmin, like tPA

47
Q

what regulates plasmin activity?

A

alpha2-antiplasmin

48
Q

heparin-like molecule

A

activates antithrombin which inhibits thrombin

49
Q

difference in fibrinolysis and anti-thrombosis

A

fibrinolysis = breakdown of fibrin clot

anti-thrombosis = clot never forms to begin with

50
Q

What is another term for thrombin?

A

factor II

51
Q

What else does heparin inhibit, in addition to thrombin?

A

factor X

52
Q

protein C/S network

A

inactivates Va and VIIIa and thereby quells the common/intrinsic pathways for coagulation

53
Q

heparin

A

anticoagulant

combines with antithrombin to inhibit the activity of thrombin and Xa

54
Q

What type of drug is aspirin?

A

NSAID

55
Q

clopidogrel

A

antiplatelet

blocks ADP receptors which inhibits platelet activation

56
Q

xarelto / rivaroxaban

A

anticoagulant

directly inhibits factor Xa, thus inhibiting coagulation

57
Q

warfarin / coumadin

A

anticoagulant

inhibits vitamin K-dependent clotting factor synthesis

cannot produce clotting factors in the liver

58
Q

VKORC1

A

enzyme that activates vitamin K stores in the liver

needed to synthesize clotting factors

59
Q

Virchow triad

A

endothelial injury

abnormal blood flow

hypercoagulability

*risk factors for thrombosis

60
Q

lines of zhan

A

only thrombi show lines of Zahn

blood clots lack lines of Zahn

layers of fibrin admixed with layers of aggregated platelets and blood cells

61
Q

Factor V leiden

A

in-born hypercoagulable state

factor V is resistant to inactivation by protein C+S

therefore, factor V stays on for longer and there is more clotting

62
Q

definition of embolus

A

any bolus that moves

ex: thrombosis = clot embolus

Fundamentals 2 (30 decks)

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