Anticoagulants Flashcards

1
Q

stages of hemostasis

A

vascular constriction limits blood flow to area of injury, platelets become activated by thrombin and aggregate at site of injury. Fibrinogen is responsible for stimulating platelet clumping.
Activates platelets release ADP and TXA2 which activate additional platelets, serotonin, phospholipids, lipoproteins, and other proteins important for coag cascade. Activated platelets change their shape to accommodate the formation of the plug. A fibrin mesh forms and entraps the plug. If it contains only platelets it is a white thrombus, if it contains red it is a red thrombus.
Plasmin will cause dissolution of the clot to allow issue repair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

adhesion of the platelets

A

damage to the endothelial surface> subendothelial collagen exposure
production/ release of vWF from endothelial cells.
vWF anchos platelets to subendothelial collagen vascular wall
Von Willebrands Disease most common inherited coagulation defect
teatment- DDAVP releases vWF from endothelial cells also can give FFP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

activation of platelets

A

prothrombin>thrombin IIa which activates platelets
chape change and release of mediators
TX2 and ADP promote platelet aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

aggregation of platelets

A

TX2 and ADP uncover fibrinogen receptor (GPIIb/IIIa). THis allows fibrinogen I to bind to the receptor and further aggregate platelets. after platelets aggregate, fibrin in woven into platelets and cross-linked (water soluble> stable). Cross- linkage requires fibrin stabilizing factor (XIII)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

MOA of ASA and NSAIDS

A

COX 1 inhibition: reduction in TXA2 release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

clotting factors

A

all procoags are produced in the liver with the exception of the following: Tissue factor of Thromboplastin (III) released from traumatized cells. Ca++ (IV) diet and vWF vascular endothelial cells
Vitamin K dependent factors: II, VII, IX, X, protein C, and protein S

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

factor 1

A

fibrinogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

factor 2

A

prothrombin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

factor 3

A

tissue factor/ thromboplastin- vascular wall and extravascular cell membrane; released from traumatized cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

factor 4

A

calcium- diet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

factor 5

A

proaccelerin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

factor 7

A

proconvertin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

factor 8c

A

antihemophiliac factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

factor 8 vWF

A

vonwillebrands factor- vascular endothelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

factor 9

A

christmas factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

factor 10

A

stuart prower factor

17
Q

factor 11

A

plasma thromboplastin antecedent

18
Q

factor 13

A

hageman factor

19
Q

factor 13

A

fibrin stabilizing factor

20
Q

protiens

A

c and s

21
Q

extrinsic pathway

A

damage occurs from outside of vessel> triggers release of tissue factors> this comes in contact with factor 7
complexed with Ca++ on platelet> activates factor X
Tissue factor is the primary physiologic initiator of coagulation
measured by PT test

22
Q

You can buy an extrinsic pathway for

A

37 cents

23
Q

intrinsic pathway

A

initiated when there is trauma to the vessel itself or exposure of blood to collagen.
Activation of XII>XI>IX when complexed with on platelet surface with factor VIII:C and Ca++> factor X
Measured with PTT

24
Q

you can buy the intrinsic pathway for

A

$12 or $11.98

25
Q

Common pathway

A

activation starts with factor X>V>II>I>XIII
thrombin converts fibrinogen I to fibrin and in the presence of XIII, fibrin cross linking occurs
the clot is now formed

26
Q

antithrombin 3

A

produced in the liver and neutralizes the final common pathway factors IIa & Xa and intrinsic factors IX, XIa, and XIIa
strongly inhibits factors IIa and Xa
partially inhibits factors IXa, XIa, and XIIa
Required cofactor for Heparin
heparin binds to antithrombin !!! and enhances AT !!! by 1000 times

27
Q

drugs that inhibit clotting factor synthesis

A

warfarin

28
Q

drugs that inhibit thrombin

A

heparin, lepirudin

29
Q

antiplatelet drugs

A

ASA- inhibits cyclooxygenase; duration of action is life of platelet (due to the covalent bond sharing of electron
NSAIDS_ same as ASA but the depression of TXA2 is shorter 24-48 hours
Ticlid, PLAVIX, and Persantine- inhibits ADP
Integrilin, Reopro, Aggrastat- anti-fibrinogen receptor (GPIIb/IIIa)

30
Q

thrombolytics

A

tPa, streptokinase

31
Q

antofibrinolytics

A

aprotinin(not used), Amicar used in CPB and acute hemorrhage

32
Q

heparin

A

binds/activates antithrombin III which then inhibits the serine proteases of the coag cascade. Heparin is abundant in granules of the mast cells that line vasculature. In response to injury heparin is released and inhibits coags. Heparin is also present in basophils and liver

33
Q

Coumadin

A

inhibits the vitamin K- dependent y-carboxylation reactions necessary to the function of thrombin, and factors II, VII, IX, and X as well as protein C

34
Q

ASA

A

inhibiting the activity of cyclooxegenase, aspirin reduces the production of thromboxane (TXA2). ASA also reduces endothelial cell production of prostacyclin, an inhibitor of platelet aggregation and a vasodilator. Since endothelial cells regenerate active cyclooxygenase faster than platelets. the net effect of ASA is more in favor of endothelial cell mediaated inhibition of the coag cascade.

35
Q

ReoPro, Integrellin, Aggrastat

A

glycoprotein IIb/IIIa inhibitors in the membrane of platelets, inhibit platelet aggregation. used in Acute Coronary Sydrome in ACLS protocol.