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Hemostasis > Introduction to Hemostasis > Flashcards

Introduction to Hemostasis Flashcards

1
Q

What is Hemostasis?

A

Normal process of forming a mechanical barrier to blood loss at the site
of injury, while maintaining normal blood flow throughout the rest of the
body.

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2
Q

Thrombosis

A

– Formation of a thrombus (a fibrin/platelet mass sometimes called
a ‘clot’) in vivo within a vessel

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3
Q

Embolism

A

When a small piece of a thrombus (called an ‘embolus’) breaks
off and travels through circulation, becoming lodged in a smaller
vessel leading to blood flow obstruction

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4
Q

3 Body systems in Hemostasis

A

Platelets
Vasculature
Plasma Proteins

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5
Q

3 stages of hemostasis

A

primary hemostasis
secondary hemostasis
fibrinolysis

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6
Q

Vascular system

A

Veins
Arteries
Capillaries

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7
Q

3 Layers of blood vessels

A

Tunica intima
Tunica media
Tunica adventitia

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8
Q

What 2 systems are involved in primary hemostasis? and how?

A

Platelets form primary hemostatic plug

vasculature through vasoconstriction, endothelial cell activation w/ collagen

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9
Q

Endomitosis

A

Megakaryocytes multiply INSIDE the cell to produce many platelets (16N, 32N)

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10
Q

Lifespan of platelet

A

9-12 days

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11
Q

zones of a platelet

A

Peripheral zone
structural zone
organelle zone
Membrane zone

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12
Q

Peripheral zone

A

purpose: adhesion+ aggregation
components: glycocalyx
membrane
receptors (GP1bIX - vWF)
(GP2b3a - Firbinogen)

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13
Q

Structural Zone

A

fucntion: structure and support
Components: microtubules - tubulin
protein network
Actin (G+F)

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14
Q

Organelle Zone

A

Function: secretion and storage
Components: Granules,
- Dense Bodies
- Alpha Granules

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15
Q

Components of dense granules

A

ADP
Ca2+
Serotonin

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16
Q

Alpha granules

A

vWF
Fibronectin
Fibrinogen
Factor V

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17
Q

Membrane zone

A

function: secretion and storage, regulate Ca
Components: Open Canalicular System(OCS)
Dense Tubular System (DTS)

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18
Q

Steps in Primary Hemostasis

A

Adhesion
Aggregation
Secretion
Activation

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19
Q

Platelet Adhesion

A

Collagen
Von Willebrand Factor
GP1b/IX

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20
Q

Platelet Activation

A

Biochemical changes and shape changes

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21
Q

Phospholipase C Pathway

A

PLC + PIP2 ——> IP3 + DAG
IP3, release Ca from DTS
DAG —– PKC —– Granlue secretion, GP2b3a

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22
Q

cAMP Pathway

A

Negative regulator of biochemical platelet change

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23
Q

Arachidonate Pathway

A

ADP + Ca —–> PLA2
PLA2 —-> liberates arachadonic acid
Cyclo-oxygenase —- converts AA —> PGG2
PGG2 + Thromboxane synthetase —-> Thromboxane A2

24
Q

Where does aspirin prevent clots?

A

Aspirin is a cyclo-oxygenase antagonist

25
Q

Platelet shape change

A 
Spherical + Pseudopods
centralization of granules
increase surface area
more contact w/ tissue and platelts
GP1b/IX internatlized
GP2b3a comes to surface
26
Q

Platelet Aggregation

A

GP11b/IIIa binds Fibrinogen and acts as protein bridge between platelets for the primary hemostatic plug

27
Q

Platelet Secretion

A

Shape change moves granules to center
granules fuse w/ OCS and release through exterior
granules are agaonists —- POSITIVE FEEDBACK

28
Q

Extrinsic Pathway

A

TF
Factor VII

Extrinxic Xase complex
Measured with PT test

29
Q

Intrinsic Pathway

A

Factor XII
Factor XI
Factor IX
Ca

Intrinsic Xase complex
Measured with PTT test

30
Q

Common Pathway

A

Factor X
Factor V
Prothrombin
Firbinogen

Measured by PT and PTT

31
Q

Contact Factors

A

Factor XI
Factor XII
PK
HK

32
Q

Prothrombin Group

A

Vitamin K Dependent, stable

Prothrombin
Factor VII 
Factor IX
Factor X
PRotein C + Protein S
33
Q

Fibrinogen Group

A

Acted on by thrombin, unstable

Fibrinogen
Factor V
Factor VIII
Factor XIII

34
Q

Extrinsic Xase complex

A

Activates Factor X

Can activate Factor IX (intrinsic pathway)

35
Q

Intrinsic Pathway

A 
Factor XII
Factor XI
Factor IX
VIIIa
Ca
36
Q

Extrinsic Pathway

A

Vessel Injury
TF
Factor VII

37
Q

Common Pathway

A 
Factor X
Factor V
Ca
Prothrombin
Thrombin
XIII
Fibrinogen
Fibrin
38
Q

Hemophilia A

A

Factor VIII deficiency on X chromosome

39
Q

Hemophilia B

A

Factor IX deficiency on X chromosome

40
Q

Von Willebrand Factor

A

Bridge between platelets in primary hemostatic -plug
stabilizes factor VIII
stored in alpha granules and EC’s

41
Q

Fibrinolysis steps

A

Plasminogen binds to fibrin
t-PA binds to fibrin and converts plasminogen to plasmin
plasmin digests fibrin in to soluble products

42
Q

Physiological activators of fibrinolysis

A

tPA

uPA

43
Q

Contact Activators of Firbinolysis

A

Kallikrein
Factor FXIIa
Factor FXIa

44
Q

Exogenous Activators

A

Streptokinase

Staphylokinase

45
Q

Fibrinolysis Inhibitors

A 
PAI-1
PAI-2
TAFI
alpha 2 antiplasmin (AP)
alpha 2 macroglobulin
46
Q

Mechanisms of control

A
  1. Blood Flow
  2. Liver Clearance
  3. Positive/Negative Feedback
  4. Biochemical Inhibitors
47
Q

Positive feedback

A

Thrombin

Factor Xa

48
Q

Negative Feedback

A

Thrombin
TFPI
Fibrin
FDP’s

49
Q

Biochemical inhibitors

A

Antithrombin (AT)Heparin Cofactor II (HCII)

50
Q

Antithrombim (AT)

A

Inhibits serine proteases
thrombin
FVIIa, FXIIa, FXIa, FIXa, FXa, PK

Heparin ACCELERATES Antithrombin

51
Q

Heparin Cofactor II (HCII)

A

Inhibits thrombin
Heparin aids (but less than AT)
Accelerated by dermatan sulfate

52
Q

Protein C

A

Inhibits Va, Viiia

53
Q

Protein S

A

Cofactor for Protein C

54
Q

APC/APS Pathway

A 
Injury ---- thrombin from EC's 
Excess thrombin binds Thrombomodulin
T/TM complex activates Protein C
APC binds PS
APC/PS inhibits FVa, FVIIIa
55
Q

Factor V Leiden

A

Protein C and Protein S cant bind APC/PS to FV

INHIBITOR OF INHIBITION

DOUBLE NEGATIVE

56
Q

Tissue Pathway Factor Inhibitor (TFPI)

A

Inhibits Xa, and Viia/TF

Hemostasis (3 decks)

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