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AP2 > Hemostasis > Flashcards

Hemostasis Flashcards

1
Q

What are the 3 phases of hemostasis

A

Primary-formation of a plug

Secondary=coagulation

Tertiary-fibrinolysis

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2
Q

What is von willebrand factor?

A

vWF is a large, heterogeneous multimeric glycoprotein that protects factor VIII from rapid inactivation

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3
Q

how does von willebrand factor bind?

A

binds platelets via the glycoprotein Ib receptor complex

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4
Q

What makes vWF bind to platelets?

A

Change in shear rate.

Inactive vWF is globular.

As flow of blood is changed due to injured epithelium it opens into an extended chains exposing the glycoprotein Ib receptor complex

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5
Q

What two substances account for platelet adhesion?

A

vWF via gycoprotein Ib receptor.

collagen when exposed the gycoprotein VI receptor and a2b1 integrin on the platelet bind to the collagen

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6
Q

What is von Willebrand’s disease?

A

vW disease is the most common congenital bleeding disorder. It manifests as impaired platelet function.

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7
Q

What is the treatement for vW disease?

A

DDAVP–expresses vWF so may be usied for mild cases.

Humate-P is concentrated vWF/factor VIII, and is a go too.

Other treatments are FFP and cryoprecitipate.

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8
Q

What causes platelets to become activated?

A

Agonists at the site of injury.

Collagen and Thrombin are the most common.

Others included ADP and epinephrine.

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9
Q

What happens during platelet activation?

A

Platelets change morphology

They then release the contenst of their alpha granules and dense granules. These included ADP, serotinin, factor V, factor VIII, vWF, fibrinogen

Also substances s.a. thromboxaneA2 synthesiszed in the cytosol are released into the environment

New negatively-charged receptors are expressed on their surface membrane

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10
Q

How does aspirin stop platelet aggregation?

A

blocks cyclooxygenase enzymes, which lead to the formation of thromboxane from arachidonic acid. Thromboxane signals platelet aggregation. Moreover aracodonic acid converts to prostaglandin via the the cox-2 enzyme. this illustrates the connection between inflammation and platelet aggregation.

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11
Q

What receptors are on the platelets surface?

A

Thrombin-> Protease-activated receptors PAR1 and Par4

ADP->P2Y1 and P2Y12.

Fibrinogen-> glycoprotein IIb/IIIa

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12
Q

What may block the ADP receptors on platelets?

A

thienopyridines: ticlopidine and clopidogrel

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13
Q

What may block the fibrinogen receptors on platelets?

A

antagoists such as abciximab and tirofiban

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14
Q

What are the primary adhesive molecules for platelet aggregation?

A

Fibrinogen and vWF

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15
Q

Which platelet surface receptor mediates platelet aggregation?

A

glycoprotein IIb/IIIa receptor

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16
Q

How do fibrinogen and vWF cause platelet aggregation?

A

form bridges between platelets to create a plug

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17
Q

What is the sequence from a resting platelet to platelet aggregation?

A

GPIIb/IIIa receptors are in a ligand unreceptive state in the resting platelet.

In the presence of an agonist (ADP, thrombin, epinephrine) the platelet becomes activated and is ready to accept a ligand.

With fibrinogen present, the fibrinogen binds to the activated GPIIb/IIIa receptors. These form bridges with other fibrinogen bound platelets

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18
Q

What is the order of fibrinogen in a primary hemostatis?

A

fibrinogen->fibrin monomers->fibrin polymers

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19
Q

which factor is fibrin stabilizing factor?

A

Factor XIII

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20
Q

How does Aspirin affect fibrinogen and FXIII

A

Aspirin acetylates fibrinogen causing the clot structure to be looser and easier to lyse

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21
Q

how are most coagulation factors found in circulation?

A

inactive forms-proenzymes or zymogens. A portion is cleaved off to activate the coagulation factor

22
Q

What is the necessary factor for proper interaction of coagulation factors?

A

presence of a negatively-charged phopholipid membrane

23
Q

Where are (most) coagulation factors synthesized

A

liver

24
Q

Which are the contact activation factors?

A

FXI and FXII

25
Q

Which is the only factor that has extra hepatic origin?

A

FVIII

26
Q

What are the Vit K dependent factors?

A

FII, FVII, FIX, and FX

27
Q

What are the two portion of FVIII?

A

High molecular weight portion-carrier.

small molecular weight–coagulant activity

28
Q

What reaxtion does vitamin k catalyze?

A

the carboxylation of glutamic acid glutamic acid->gamma-caroxyglutamic acid it is also possible for the factor to bind calcium

29
Q

How is vitamin K found in the diet?

A

leafy greens-kale

30
Q

What inhibits carboxylation of vitamin K dependent factors by vitamin K?

A

coumadin

31
Q

Which of the vitamin K dependent factors has the shortes half life?

A

FVII

32
Q

What is hemophilia A?

A

Deficiency of FvIII

33
Q

What is Hemophilia B?

A

Deficiency of FIX

34
Q

What are the hemostatic actions of thrombin in the cascade based model?

A

Cleaves fibrinogen to fibrin activates factor XIII to cross-link fibrin Activates Platelets Activats factors V, VII, VIII, IX Activates thrombin activatable fibrinolysis inhibitor Stimulates epithelial cells to produce TF and vWF stimulates subendothelial smooth muscle constriction

35
Q

Which are the most importent factors in clotting?

A

VIII, and IX

36
Q

What are teh stages of the cell based model of coagulation?

A

Initiation-procoagulant stimulus generates engough trombin to initiate the coagulation process Amplification: Platelects and coagulation factors are activated Propagation: large amounts of thrombin are generated on the activated platelet surface

37
Q

What happens during initiation?

A

On the tissue factor bearing cell, just a liitle bit o thrombin is form. If enough is formed then the next step will begin

38
Q

What happens during amplification?

A
39
Q

What happens during propagation?

A
40
Q

What is all the thrombin in the clell based model for?

A

Cleavage fo fibrinogen to fibrin

Activates factor XIII to cross-link fibrin

Activates platelets

activates V, VII, VIII, IX

Activate thrombin activatable fibrinolysis inhibitor

Stimulates epithelial cells to produce TF and vWF

Stimulates subendothelial smooth muscle contriction

41
Q

How is coagulation regulated?

A

Tissue factor pathway inhibitor (TFPI): inhibits TF/FVIIa complex and TF/FVIIa/FXa complex

Antithrombin (AT) inhibits FXa and thrombin (this is the biggest regulator in adults)

Protein C (PS) with cofactor protein S inhibits FVa and FVIIIa

42
Q

What is the role of heparin in coagulation?

A

Its primary anticoagulant action is its ability to inhibit thrombin activity

Binds to AT and causes a conformational change in the molecular structure of AT that transforms AT from a slow to rapid inhibitor of throm

43
Q

Which step is tertiary hemostasis and how does it work?

A

fibrinolysis

44
Q

how do neonates differ from adults in coagulant and anti coagulant factors

A

neonates have low leves of both procoagulant factors and anticoagulant factors, nevertheless neonates have a well balanced, efficient hemostatic system

(Vitamin K dependent factors, contact activation factors and coagulant inhibitors)

45
Q

HOw do platelets differ in neonates vs adults?

A

Neonates have 100% of adult platelets with fully developed membrane glycoprotein expression.

however, tehese platelets contain half the amount of dense granules, and platelet aggregation is impaired in responding to ADP, EPI, collagen and thrombin. However, they still have efficient platelet function.

This is due to an increased concentraition of von Willebrand factor and increased number of large vWf multimers.

46
Q

how is fibrinogen different in neonates vs adults

A

Neonatal fibrinogen is 100% adult value but it has a different chemical structure whci gives it a decreased rate of fibrin polymerization and the fibrin clot is characterized by a lower density. This fetal form of fibrinogen exists until 1 year of age.

47
Q

how is neonatal plasminogen differnt from adult

A

Plasminogen in neonates is found to be 50% adult values. Further i has decreased functional activity due to a different chemical structure causing it to bind poorly to cellular receptors. Also the activation kinetics by tissue plasminogen activator are slow and inhibition kinetics by antiplasmin a2 are slower.

Overall neonatal plasminogen has less fibrinolytic activity because of both quantitative and qualitative deficiencies in plasminogen.

48
Q

What are the FDA approved uses of Recombinant actvated factor VII?

A

Pts with hemophila A and B with inhibitors aganst FVIII and FIX

Pts with congential FVII deficiency for Tx of blleding , or prevention of bleeding during surgical or invasive procedures

49
Q

What are the off label uses of Recombinant activated factore VII?

A

Liver failure

liver transplantation

drug induced cagulopathies

platelet disorders

renal failure

intracerebral hemorrhage

non-hemophiliac bleeding disorders

Intraoperative or postoperative hemostasis

Bleeding due to trauma

Post cardiopulmonary bypass

50
Q

What are the disadvantages of rFVIIa?

A

It is very expensive-pt chare $2738

No accepted standard monitor for efficacy

Unknown safety

JAMA article–most thromboembolic events occured among off label uses (CVA, MI, arterial thrombses, PE)

51
Q

What is the mechanism of action of rFIIa?

A

IN initiation FVIIa drives the reaction forward to ensure enough thrombin is formed to make push into amplification.

In propagation, in high doses it binds to activated platelet and activates FX bypassing VIII and IX such as in hemophilia

AP2 (2 decks)

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