Ios V Exam 1

Front 1

during the activation stage of platelets in hemostasis, what substances does the platelet release? what do these substances do?

Back 1

EPI, TXA and ADP. they recruit more platelets to site of injury and also cause conformational change of the platelets.

Front 2

what is the name of the platelet receptor that interacts with the von willebrond factor?

Back 2

Gp1b receptor

Front 3

tissue factor plays a role in which part of the coagulation cascade, i.e. the intrinsic pathway or extrinsic pathway?

Back 3

extrinsic pathway

Front 4

which factor is involved in the conversion of prothrombin to thrombin?

Back 4

factor X

Front 5

thrombin is also known as what factor?

Back 5

factor II

Front 6

what is the name of the protein that breaks down fibrin?

Back 6

plasmin

Front 7

which of the following is considered thrombogenic?
a. thrombomodulin
b. protein C/S
c. TFPI
d. Tissue factor

Back 7

d. tissue factor

Front 8

which of the following is considered an anticoagulant?
a. turbulent blood flow
b. TFPI
c. plasminogen activator inhibitor-1
d. vWF (von willebrand factor)

Back 8

b. TFPI (tissue factor pathway inhibitor)

Front 9

how does plasminogen activator inhibitor-1 inhibit clot degradation?

Back 9

by binding to tissue plasminogen activator directly, and deactivating it.

Front 10

what are the targets of anti-thrombin?

Back 10

factors IIa, IXa, and Xa

Front 11

what factors does protein c inactivate?

Back 11

factors Va and VIIIa

Front 12

"pathologic process leading to inappropriate clot formation. can occur in arteries or veins" is the definition of what?

Back 12

thrombosis

Front 13

antiplatelet drugs play a bigger role in which type of clot (i.e. arterial or venous)?

Back 13

arterial clot. since arterial thrombi are composed mostly of platelets.

Front 14

anticoagulant drugs play a bigger role in which type of clot (i.e. arterial or venous)?

Back 14

venous clot. since a venous thrombi are composed mostly of firbin and RBCs

Front 15

arterial clots form in area of ______ (rapid/slow) blood flow.

Back 15

rapid blood flow (arterial thrombi usually form at site of vascular injury rather than stasis, which is more characteristic of venous clots).

Front 16

what are the three components that make up virchow's triad?

Back 16

venous stasis
hypercoagulability
vascular damage

Front 17

pregnancy can play a role in two parts of virchow's triad. which two parts?

Back 17

venous stasis and hypercoagulability

Front 18

inflammatory diseases can play a role in two parts of virchow's triad. which two parts?

Back 18

vascular damage and hypercoagulability

Front 19

what is the name of the most common acquired hyper-coaguable disorder?

Back 19

antiphospholipid antibody syndrome (APLA). presents as either lupus anticoagulant (LA) or anticardiolipin antibody (ACLA)

Front 20

what are three medications (there are more, but there are in particular three drugs that are highlighted on the slide...) that may lead to APLA (antiphospholipid antibody syndrome), a.k.a. drug induced lupus?

Back 20

phenytoin
hydralazine
procainamide

Front 21

what is the name of hte most common inherited disorder that causes hypercoagulability?

Back 21

activated protein C resistance (factor V leiden)

Front 22

Activated Protein C resistance (factor V leiden) is a hypercoagulability disease. this disease increases the risk of developing what type of clots (i.e. venous or arterial?(

Back 22

venous clots (increased risk of 2-3 fold compared to healthy subjects).

Front 23

why should warfarin be avoided in patients with a protein C deficiency?

Back 23

protein c is a vitamin k dependent protein made in the liver. warfarin could worsen hypercoagulable state of protein c deficiency

Front 24

what clotting factors does protein C inactivate? what cofactor does protein C require for inactivation of these clotting factors?

Back 24

factor V and factor VIII.
cofactor required: protein S

Front 25

homocystinemia is a condition in which a patient has elevated levels of homocysteine. what is the risk associated with having homocystinemia?

Back 25

increased risk for arterial and venous thrombosis.

Front 26

what does antithrombin do?

Back 26

inactivates thrombin, and other serine proteases.

Front 27

antithrombin deficiency primarily increases the risk of what type of clot? i.e. arterial or venous?

Back 27

increases risk for venous clots (rarely for arterial clots as well though)

Front 28

what is the result of prothrombin gene mutation G20210A ?

Back 28

increases prothrombin activity and levels. RR is 2-3 fold that of individuals without the condition.

Front 29

what three roles does thrombin play?

Back 29

produces fibrin
feedback amplification
stimulates platelet activation

Front 30

proteins in the endothelium repel platelets and clotting factors due to having similar charges. are these proteins negatively or positively charged?

Back 30

negatively charged

Front 31

heart failure and atrial fibrillation are located under which category of virchow's triad?

Back 31

venous stasis - abnormalities of blood flow

Front 32

acute MI and heart valve disease are located under which category of virchow's triad?

Back 32

vascular damage - abnormalities of surfaces in contact with blood

Front 33

hemophilia is a congenital bleeding disorder due to deficient production of which two specific clotting factors?

Back 33

factor VII and factor IX

Front 34

what is the role of calcium in the coagulation cascade?

Back 34

it is a cofactor that accelerates the cascade, in particular in the formation of thrombin from prothrombin. (i.e. it is a cofactor involved in the activity of Xa)

Front 35

besides factor Xa, what other factors and cofactors are involved in the formation of thrombin?

Back 35

factor Va, Ca++ and phospholipids

Front 36

what is the name of the residue required for coagulation factors to be fully functional?

Back 36

gamma-carboxylated glutamic acid

Front 37

what are the 4 vitamin K dependent clotting factors?

Back 37

II, VII, IX, and X

Front 38

thrombin essentially forms a soft clot by converting _____ to ______.
factor XIII forms a sturdier clot by ___________

Back 38

converting fibrinogen to fibrin

by crosslinking fibrin

Front 39

patients with which two alleles for CYP2C9 demonstrate increased bleeding risk and decreased dosing requirements for warfarin?

Back 39

2* and 3*

Front 40

filll in the blanks: 55% of the variance in warfarin dosing can be explained by three things:
1. clinical factors, such as age, height, body weight, interacting drugs, and indication
2. ______
3. ______

Back 40

VKORC1 polymorphisms
CYP2C9 polymorphisms

Front 41

do the guidelines for antithrombotic therapy suggest pharmacogenetic based initial dosing?

Back 41

no. they do not.

Front 42

in which patients will we want to initiated warfarin therapy at a lower dose of 2.5 mg daily?

Back 42

patients older than 60, malnourished, have heart failure, liver disease, recent surgery, or taking inhibiting medications

Front 43

what two substances secreted by the endothelium inhibit platelet activation?

Back 43

NO and PGI2

Front 44

platelet function and coagulation cascade are primarily linked in what way according to the cell-based model of thrombosis?

Back 44

platelets provide cell surface membrane area required for the steps in the coagulation cascade - localizaing thrombus formation to the site needed.

Front 45

the cell-based model of thrombosis is described in three phases. what are those three phases?

Back 45

1. initiation phase
2. amplification
3. propagation

Front 46

trauma surgery is listed under what portions of virchow's triad?

Back 46

stasis, vessel wall damage and hypercoagualbility (i.e. all 3)