Introduction to Hemostasis Flashcards

(56 cards)

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
Platelet shape change
``` Spherical + Pseudopods centralization of granules increase surface area more contact w/ tissue and platelts GP1b/IX internatlized GP2b3a comes to surface ```
26
Platelet Aggregation
GP11b/IIIa binds Fibrinogen and acts as protein bridge between platelets for the primary hemostatic plug
27
Platelet Secretion
Shape change moves granules to center granules fuse w/ OCS and release through exterior granules are agaonists ---- POSITIVE FEEDBACK
28
Extrinsic Pathway
TF Factor VII Extrinxic Xase complex Measured with PT test
29
Intrinsic Pathway
Factor XII Factor XI Factor IX Ca Intrinsic Xase complex Measured with PTT test
30
Common Pathway
Factor X Factor V Prothrombin Firbinogen Measured by PT and PTT
31
Contact Factors
Factor XI Factor XII PK HK
32
Prothrombin Group
Vitamin K Dependent, stable ``` Prothrombin Factor VII Factor IX Factor X PRotein C + Protein S ```
33
Fibrinogen Group
Acted on by thrombin, unstable Fibrinogen Factor V Factor VIII Factor XIII
34
Extrinsic Xase complex
Activates Factor X | Can activate Factor IX (intrinsic pathway)
35
Intrinsic Pathway
``` Factor XII Factor XI Factor IX VIIIa Ca ```
36
Extrinsic Pathway
Vessel Injury TF Factor VII
37
Common Pathway
``` Factor X Factor V Ca Prothrombin Thrombin XIII Fibrinogen Fibrin ```
38
Hemophilia A
Factor VIII deficiency on X chromosome
39
Hemophilia B
Factor IX deficiency on X chromosome
40
Von Willebrand Factor
Bridge between platelets in primary hemostatic -plug stabilizes factor VIII stored in alpha granules and EC's
41
Fibrinolysis steps
Plasminogen binds to fibrin t-PA binds to fibrin and converts plasminogen to plasmin plasmin digests fibrin in to soluble products
42
Physiological activators of fibrinolysis
tPA | uPA
43
Contact Activators of Firbinolysis
Kallikrein Factor FXIIa Factor FXIa
44
Exogenous Activators
Streptokinase | Staphylokinase
45
Fibrinolysis Inhibitors
``` PAI-1 PAI-2 TAFI alpha 2 antiplasmin (AP) alpha 2 macroglobulin ```
46
Mechanisms of control
1. Blood Flow 2. Liver Clearance 3. Positive/Negative Feedback 4. Biochemical Inhibitors
47
Positive feedback
Thrombin | Factor Xa
48
Negative Feedback
Thrombin TFPI Fibrin FDP's
49
Biochemical inhibitors
Antithrombin (AT)Heparin Cofactor II (HCII)
50
Antithrombim (AT)
Inhibits serine proteases thrombin FVIIa, FXIIa, FXIa, FIXa, FXa, PK Heparin ACCELERATES Antithrombin
51
Heparin Cofactor II (HCII)
Inhibits thrombin Heparin aids (but less than AT) Accelerated by dermatan sulfate
52
Protein C
Inhibits Va, Viiia
53
Protein S
Cofactor for Protein C
54
APC/APS Pathway
``` Injury ---- thrombin from EC's Excess thrombin binds Thrombomodulin T/TM complex activates Protein C APC binds PS APC/PS inhibits FVa, FVIIIa ```
55
Factor V Leiden
Protein C and Protein S cant bind APC/PS to FV INHIBITOR OF INHIBITION DOUBLE NEGATIVE
56
Tissue Pathway Factor Inhibitor (TFPI)
Inhibits Xa, and Viia/TF