Hepatic Quiz 2

Front 1

What is average life span platelet?
Normal platelet count?

Back 1

8-12 days
150,000-400,000

Front 2

Approximately how much of platelet pool is sequestered in the spleen?

Back 2

33%

Front 3

Active factors of platelets in cytoplasm are/

Back 3

actin
myosin
thrombosthenin(contractile protein)

Front 4

Platelets cell surface is?
This resists adherence to normal endothelium, and adheres to injured endothelial cells.

Back 4

coat of glycoproteins

Front 5

What are the four mechanisms in primary hemostasis?

Back 5

adhesion
activation
aggregation
fibrin production

Front 6

What is the mechanism of action of adhesion?

Back 6

When vascular endothelium is damaged, the sunendothelium layer of the blood vessel wall is exposed and von Willebrand or factor VIII anchors platelets to the collagen layer of subendothelium. This promotes platelet adhesion

Front 7

What is the most common inherited coagulation defect?

Back 7

vWF, should be suspected in any patient with an increased bleeding time despite a normal platelet count and normal clot reaction

Front 8

What is the treatment for vWF?

Back 8

Desmospression-cause release of endogenous vWF, TPA, and prostaglandings, should work in 30min
Cryoprecipitate-can increase vWF, Has factor VIII, I(fibrinogen), and factor XIII
Factor VIII concentrate-pooled plasma product that inactivates HIV and hepatitis

Front 9

Activation of platelets occurs how?

Back 9

Thrombin (activated factor II or factor IIa) combines with thrombin receptor on platelet surface to activate the platelet
Involves shape change in platelet and release of mediators involved in coagulation and healing
Thromboxane A2 and ADP are mediators synthesized and released from the activated platelet and these promote platelet aggregation.

Front 10

How does aggregation of platelets occur?

Back 10

Thromboxane A2 and ADP uncover fibrinogen receptors
Fibronogen attaches to receptors and links platelets to one another
Fibrinogen (Factor 1) aggregates platelets to the site of injury where they form the first hemostatic plug

Front 11

Why does aspirin cause appregation disorder?

Back 11

cyclo-oxygenase is rendered non-functional bc the acetyl group of aspirin causes acetylation of cyclo-oxygenase and this presists for the life of the platelet(8-12 days)
Cyclo-oxygenase is the rate limiting enzyme in the conversion of arachidonic acid to the thromboxane A2. Without thromboxane A2 platelt aggregation is impaired.

Front 12

How does NSAID's cause aggregation disorders?

Back 12

same as aspirin, but depression of thromboxane A2 production by platelets is temporary -only 24-48 hrs, not permanent

Front 13

What is the most commonly acquired blood clotting defect due to?

Back 13

inhibition of cyclo-oxygenase production by aspirin or NSAIDS

Front 14

What is the MOA of platelets?
What is MOA of antiplatelet drugs?

Back 14

Thrombin activates platelet
Phospholipase converts a membrane phospholipid to Arachodonic Acid
Cyclo oxygenase converts arachodonic acid to Prostaglandin G2
Prostaglandin G2 is metabolized into a variety of prostaglandins including thromboxane A2
ASA and NSAIDS interfere with the synthesis of thromboxane A2 by interfering with cyclo-oxygenase

Front 15

How is the production of Fibrin form a clot?

Back 15

After platelets aggregate, thrombin also produces Fibrin at the site of injury
Fibrin is woven into platelts and cross linked
Cross linking fibrin strands reuires factor XIII
Factor XIII and Fibrin tighten up to the platelet plug-secondary hemostasis

Front 16

Why is the extrinsic pathway initiated and what are the factors involved and general steps?

Back 16

Initiated in response to damage occuring outside the blood vessel
Thromboplastin is released which activates VII, VII and Ca IV complex on the surface of the platelet with thromboplastin which activates X,
The factors involved are III and VII

Front 17

Why is intrinsic pathway iniated and what are factors involved and steps?

Back 17

Initiated by damage inside the blood vessel.
Factors are VIII, IX, XI, XII
XII activates XI which activates IX which activates IX which forms complex on platelet surgace with VII which activates factor X

Front 18

What are the coagulation factors of the final common pathway?

Back 18

I, II, V, X, XIII

Front 19

Fibrin cross linking occurs in the presence of what?

Back 19

XIII, important secondary hemostatis

Front 20

Coumadin interferes with what and what assesses this?

Back 20

Interferes with extrinsic pathway,
PT and INR assess extrinsic pathway

Front 21

What does heparin interfere with and what assess this pathway>

Back 21

Heparin interferes with this pathway,
PTT and ACT assess this

Front 22

What is the primary physiologic initiator of coagulation and what interferes with this?

Back 22

Thromboplastin,
heparin inhibits

Front 23

Sex linked recessive genetic disorder that effects males more than females, Factor VIII, c deficiency?
Treatment?

Back 23

Hemophilia A\
Treat with fresh frozen plasma and cryoprecipitate

Front 24

Christmas disease, factor IX deficiency, treatment?

Back 24

Christmas disease, Hemophilia B
Heat treated, concentrated preparations of factor IX

Front 25

What is the best measurement of platelet function?

Back 25

Bleeding time

Front 26

What is the most common reason for coagulopathies in patients receiving massive blood transfusions?

Back 26

lack of functioning platelets, also dilution of factors V and VII

Front 27

What is the only acceptable clinical indication for transfusion of packed red cells?

Back 27

to increase the oxygen carrying capacity of blood

Front 28

Cryoprecipitate contains what?

Back 28

I, VII, XIII

Front 29

What facots in FFP?

Back 29

all pro coagulants

Front 30

What is responsible for anticoagulation? Where made and how works?

Back 30

antithrombin III
Made in liver
Neutralizes final common pathway factors IIa, Xa
Intrinsic pathway factors IX, XI, XII
Forms complexes with them
Binds thrombin, removes them from circulation
Strongly inhibits thrombin(factor IIa) and Xa
Partially inhibits factors IX, XI, XII

Front 31

how does Heparin work with Antithrombin III?

Back 31

Antithrombin III is a required cofactor for heparin, bind together
When heparin attached, the rate of reaction increases 1,000 fold

Front 32

What is the most common reason patients are unresponsive to heparin?

Back 32

Antithrombin III deficiency, FFP can teat

Front 33

What factors are depressed by heparin?

Back 33

Factors thrombin II, X, IXa, XIa, XIIa

Front 34

What is prolonged by heparin, what does it block, what reverses heparin?

Back 34

PTT is prolonged
Heparin blocks intrinsic and final common pathway
Protamine reverses action by neurtralization

Front 35

How does warfarin work and what is prolonged?

Back 35

Warfarin bind to vitamin K receptors in liver and competitively inhibit Vitamin K
Production of vitamin dependent clotting factors (II, VII, IX, and X) are depressed
PT is prolonged
Block extrinsic and final common pathway

Front 36

What are Vitamin K dependent clotting factors?

Back 36

II, VII, IX, and X

Front 37

What destroys clots and how does it work?

Back 37

Plamin
Plasminogen, the inactive form, is synthesized in liver and circulated in the blook, and is incororated into a clot as the clot is formed
Tissue type lasminogen activator or TPA and urokinase-type plasminogen activator or UPA are the two agents that normally convert plasminogen into its active form, plasmin
Plasmin breaks down fibrin

Front 38

What are the plasminogen activators and how do they work?

Back 38

TPA-produced endothelial cells and released into circulation
Release is stimulated by thrombin and venous statis
TPA by binding to fibrin, converts plasminogen to plasmin within the thrombus
UPA-found limited amount in blood
little affinity for fibrin
Urokinase is the most widely used thrombolytic agent for inta arterial infuciton into the peripheral arterial system and grafts
Streptokinase
Is produced by B-hemolytic streptococci
Streptokinase has little affinity for fibrin, preformed antibodies to streptokinase my inactivate it

Front 39

Antifibrinolytic agent, inhibits plasmin, so firbin breakdown is slowed, used during cardiac surgery to decrease bleeding

Back 39

Aprotinin

Front 40

Prevents the breakdown of fibrin by preventing the attachment of plasmin to fibrin, beneficial in the control of hemorrhage associated with primary fibrinolysis casused by increase plasminogen activation

Back 40

Amicar

Front 41

Inhibits ADP induced fibrinogen aggregation of platelts for the life of the platelet

Back 41

Ticlopidine

Front 42

Increase c-AMP in platelets and this prevents aggreatation of platelts. Used in combo with coumdadin to treat patients with prosthetic heart valves

Back 42

Dipyridamole

Front 43

Inhibits ADP induced fibrinogen aggregation of platelets for the life of the platelets

Back 43

Clopidogrel

Front 44

These drugs block fibrinogen from binding its receptor. Resultant effect is no linking of platelets, no aggregation

Back 44

Antifibrinogen receptor BPllb/llla agents
integrillin, reopro, aggrestat